Diagnosis and Management of Lameness in the Horse 2nd ed (Ross & Dyson)

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Mike W. Ross, DVM, Dipl ACVS Professor of Surgery Department of Clinical Studies University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania, United States

Sue J. Dyson, MA, VetMB, PhD, DEO, FRCVS Head of Clinical Orthopaedics Centre for Equine Studies Animal Health Trust Newmarket Suffolk, England

3251 Riverport Lane St. Louis, Missouri 63043

DIAGNOSIS AND MANAGEMENT OF LAMENESS IN THE HORSE Copyright © 2011, 2003 by Saunders, an imprint of Elsevier Inc.

ISBN: 978-1-4160-6069-7

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Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Diagnosis and management of lameness in the horse / [edited by] Mike W. Ross, Sue J. Dyson. – 2nd ed.     p. ; cm.   Includes bibliographical references and index.   ISBN 978-1-4160-6069-7 (hardcover : alk. paper)  1.  Lameness in horses.  I.  Ross, Mike W.  II.  Dyson, Sue J.   [DNLM:  1.  Horse Diseases.  2.  Lameness, Animal.  3.  Horses–injuries. SF 959.L25]   SF959.L25R67  2011   636.1’089758–dc22 2010035776

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Contributors

Rick M. Arthur, DVM

Equine Medical Director School of Veterinary Medicine University of California, Davis Davis, California

Greg Baldwin, BSc, BVSc

Australian Equine Laminitis Research Unit School of Veterinary Science The University of Queensland Queensland, Australia

Lance H. Bassage II, VMD, DACVS Staff Surgeon Rhinebeck Equine, LLP Rhinebeck, New York

Andrew P. Bathe, MA, VetMB, DEO, DECVS, MRCVS Partner, Head of Equine Sports Injuries Clinic Rossdale Diagnostic Centre Rossdale and Partners Newmarket, Suffolk, United Kingdom

Jill Beech, VMD, DACVIM

Georgia E. and Philip B. Hofmann Professor of Medicine and Reproduction Department of Clinical Studies University of Pennsylvania New Bolton Center Kennett Square, Pennsylvania

Scott D. Bennett, DVM Equine Services Clinic Simpsonville, Kentucky

Jeff A. Blea, DVM

President Southern California Equine Foundation Arcadia, California Partner Von bluecher, Blea, Hunkin, Inc. Sierra Madre, California

Jane C. Boswell, MA, VetMB, Cert VA, Cert ES(Orth), DECVS, MRCVS Partner The Liphook Equine Hospital Liphook, Hampshire United Kingdom

Robert P. Boswell, DVM

Equine Sports Medicine and Diagnostic Imaging Wellington, Florida

Robert M. Bowker, VMD, PhD Professor College of Veterinary Medicine Michigan State University East Lansing, Michigan

Julia Brooks, DO, MSc

Haywards Heath and Burgess Hill Osteopathic Practices West Sussex, United Kingdom

Herbert J. Burns, VMD Pine Bush Equine Pine Bush, New York

John P. Caron, DVM

Clinique Equine Les Breviaires, France

Professor, Equine Surgery Large Animal Clinical Sciences Michigan State University East Lansing, Michigan

William V. Bernard, DVM, DACVIM

G. Kent Carter, DVM, DACVIM

Philippe H. Benoit, DVM, MS

Owner/Manager Lexington Equine Surgery Lexington, Kentucky

Alicia L. Bertone, DVM, PhD, DACVS

Trueman Family Endowed Chair and Professor Veterinary Clinical Sciences The Ohio State University Columbus, Ohio

Jerry B. Black, DVM

Professor College of Veterinary Medicine Texas A & M University College Station, Texas

Eddy R.J. Cauvin, DVM, MVM, PhD, HDR, CertVetRad, DECVS Azurvet Hippodrome de la Côte d’Azur Cagnes-Sur-Mer, France

Director of Undergraduate Programs Equine Sciences Colorado State University Fort Collins, Colorado

Mark W. Cheney, DVM

James T. Blackford, DVM, MS, DACVS

Associate Veterinarian Manor Equine Hospital Monkton, Maryland

Professor of Large Animal Surgery Large Animal Clinical Sciences University of Tennessee College of Veterinary Medicine Knoxville, Tennessee

Veterinary Practice Lexington, Kentucky

Jennifer M. Cohen, VMD, DACVS

Chris Colles, BVetMed, PhD, HonFWCF, MRCVS Director Avonvale Veterinary Practice Banbury, United Kingdom

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Contributors

Simon N. Collins, PhD, BSc (Hons)

Australian Equine Laminitis Research Unit (AELRU) School of Veterinary Science The University of Queensland Gatton, Queensland Australia Orthopaedic Research Consultant Centre for Equine Studies Animal Health Trust Newmarket, United Kingdom

Robin M. Dabareiner, DVM, PhD, DACVS Associate Professor of Lameness Texas A & M University Large Animal Clinical Sciences College Station, Texas

Robert Andrew Dalglish, BVM&S, MRCVS Senior Veterinarian Veterinary Department Al Wathba Stables Abu Dhabi, United Arab Emirates

Elizabeth J. Davidson, DVM, DACVS Assistant Professor of Sports Medicine Department of Clinical Studies University of Pennsylvania Kennett Square, Pennsylvania

Jean-Marie Denoix, DVM, PhD, Agrégé

José M. García-López, VMD, DACVS Assistant Professor of Surgery Large Animal Surgery Department of Clinical Sciences Tufts University Cummings School of Veterinary Medicine North Grafton, Massachusetts

Ronald L. Genovese, VMD Cleveland Equine Clinic, LLC Ravenna, Ohio

Howard E. Gill, DVM Pine Bush, New York

Dallas O. Goble, DVM

Strawberry Plains, Tennessee

Nancy L. Goodman, DVM Loveland, Colorado

Barrie D. Grant, DVM

San Luis Rey Equine Hospital Bonsall, California

Kevin K. Haussler, DVM, DC, PhD, DACVSMR Assistant Professor Department of Clinical Sciences Colorado State University Fort Collins, Colorado

Professor Director CIRALE–Ecole Vétérinaire d’Alfort Goustranville, France

Dan L. Hawkins, DVM, MS, DACVS

Stephen P. Dey III, VMD

Racing Steward The Jockey Club New York Racing Association Jamaica, New York

Dey Equine Veterinarians Allentown, New Jersey

Janet Douglas, MA, Vet MB, MSc, PhD, MRCVS Special Lecturer in Equine Orthopaedics School of Veterinary Medicine and Science University of Nottingham Sutton Bonington, Nottinghamshire, England

Matthew Durham, DVM

Associate Veterinarian Steinbeck Country Equine Clinic Salinas, California

David R. Ellis, BvetMed, DEO, FRCVS Newmarket Equine Hospital Newmarket Suffolk, United Kingdom

Kristiina Ertola

Tempereen Hevosklinikka Tampere Equine Clinic Ravirata Tampere, Finland

Franco Ferrero, Med. Vet. Specialista in Patologia Equina Pontirolo Nuovo, Italy

Lisa Fortier, DVM, PhD

Associate Professor of Surgery Clinical Sciences Cornell University Ithaca, New York

David D. Frisbie, DVM, PhD, DACVS Associate Professor Department of Clinical Sciences Colorado State University Equine Orthopaedic Research Center Fort Collins, Colorado

Gainesville, Florida

W. Theodore Hill, VMD

Jukka Houttu, DVM

Tempereen Hevosklinikka Tampere Equine Clinic Ravirata Tampere, Finland

Robert J. Hunt, DVM, MS, DACVS Surgeon Davidson Surgery Center Hagyard Equine Medical Institute Lexington, Kentucky

Kjerstin M. Jacobs, DVM Private Practice Chicago, Illinois

Joan S. Jorgensen, DVM, PhD, DACVIM Assistant Professor Department of Comparative Biosciences University of Wisconsin Madison, Wisconsin

Chris E. Kawcak, DVM, PhD, DACVS Associate Professor Equine Orthopaedic Research Center Department of Clinical Sciences Colorado State University Fort Collins, Colorado

Kevin P. Keane, DVM

Member Sports Medicine Associates of Chester County Kennett Square, Pennsylvania

Contributors

Kevin G. Keegan, DVM, MS, DACVS

Professor and Director E. Paige Laurie Endowed Program in Equine Lameness Department of Veterinary Medicine and Surgery University of Missouri College of Veterinary Medicine Columbia, Missouri

John C. Kimmel, VMD Tequesta, Florida

Simon Knapp, BVetMed, MRCVS Straight Mile Farm Billingbear Wokingham Berkshire, United Kingdom

Svend E. Kold, DrMedVet, CUEW, RFP, MRCVS RCVS Specialist in Equine Surgery (Orthopaedics) Senior Consultant to B&W Equine Group Willesley Equine Clinic Tetbury, Gloucestershire, England

John Maas, DVM, MS, DACVIM

Veterinarian/Specialist in Cooperative Extension Veterinary Medicine Extension School of Veterinary Medicine University of California, Davis Davis, California

Benson B. Martin Jr., VMD, DACVS Associate Professor of Sports Medicine Dept. of Clinical Studies University of Pennsylvania New Bolton Center Kennett Square, Pennsylvania

Scott R. McClure, DVM, PhD, DACVS Associate Professor Veterinary Clinical Sciences Iowa State University Ames, Iowa

William H. McCormick, VMD, FAAVA President, CEO Middleburg Equine Clinic, Inc. Middleburg, Virginia

Andrew M. McDiarmid, BVM&S, Cert ES(Orth), MRCVS Partner Clyde Vet Group Equine Hospital Lanark, Scotland, United Kingdom

Sue M. McDonnell, PhD

University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania

C. Wayne McIlwraith, BVSc, PhD, DSc, Dr. med. vet. (hc), DSc (hc) FRCVS, DACVS University Distinguished Professor Barbara Cox Anthony University Chair in Orthopedics Director of Orthopaedic Research Center Colorado State University Fort Collins, Colorado

P.J. McMahon, MVB, MRCVS Kings Park Plaistow Billingshurst West Sussex, United Kingdom

Rose M. McMurphy, DVM, DACVA, ACVECC Professor Department of Clinical Sciences Kansas State University College of Veterinary Medicine Manhattan, Kansas

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Christopher (Kit) B. Miller Miller & Associates North Salem, New York

Martha M. Misheff, DVM Associate Veterinarian Dubai Equine Hospital Dubai, United Arab Emirates

James B. Mitchell, DVM

John R. Steele & Associates Inc. Vernon, New York

John S. Mitchell, DVM Pompano Beach, Florida

Richard D. Mitchell, DVM

President Fairfield Equine Associates, P.C. Newtown, Connecticut

Patrick J. Moloney, DVM Stuart, Florida

William A. Moyer, DVM

Texas A & M University College of Veterinary Medicine Large Animal Medicine & Surgery College Station, Texas

Graham Munroe, BVSc, PhD, DECVS, CertEO, DESM, FRCVS Flanders Veterinary Services Greenlaw Duns Berwickshire, United Kingdom

Rachel C. Murray, MA, VetMB, MS, PhD, DACVS, MRCVS Senior Orthopaedic Advisor Centre for Equine Studies Animal Health Trust Newmarket Suffolk, United Kingdom

Alastair Nelson, MA VetMB CertVR CertESM MRCVS† Rainbow Equine Clinic Rainbow Farm Old Malton Malton North Yorkshire, United Kingdom

Frank A. Nickels, DVM, MS, DACVS Professor Large Animal Clinical Sciences College of Veterinary Medicine Michigan State University East Lansing, Michigan

Paul M. Nolan, DVM Equine Sports Medicine Boca Raton, Florida

David M. Nunamaker, VMD

Jacques Jenny Professor Emeritus of Orthopedic Surgery Department of Clinical Studies University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania

Timothy R. Ober, DVM Associate Veterinarian John R. Steele & Associates Vernon, New York

†

Deceased.

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Contributors

Thomas P.S. Oliver, DVM Equine Sports Medicine Lahaska, Pennsylvania

Gene Ovnicek, RMF

President, Chief Technician Equine Digit Support System, Inc. Penrose, Colorado

Joe D. Pagan, PhD

President Kentucky Equine Research, Inc. Versailles, Kentucky

Eric J. Parente, DVM, DACVS Associate Professor of Surgery University of Pennsylvania New Bolton Center Kennett Square, Pennsylvania

Tim D.H. Parkin, BSc, BVSc, PhD, DECVPH (Population Medicine), MRCVS

Boyd Orr Centre for Population and Ecosystem Health Institute of Comparative Medicine Faculty of Veterinary Medicine University of Glasgow Glasgow, United Kingdom

Andrew H. Parks, VetMB, MRCVS, DACVS

Virginia B. Reef, DVM, ACVIM (LAIM)

Mark Whittier & Lila Griswold Allam Professor of Medicine Chief Section of Sports Medicine and Imaging Department of Clinical Studies New Bolton Center University of Pennsylvania Kennett Square, Pennsylvania

Patrick T. Reilly

Chief of Farrier Service Applied Polymer Research Laboratory University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania

Dean W. Richardson, DVM, DACVS

Charles W. Raker Professor of Surgery University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania

Mark C. Rick, DVM

Alamo Pintado Equine Medical Center, Inc. Los Olivos, California

Bradley S. Root, DVM

Albuquerque Equine Clinic Albuquerque, New Mexico

Professor of Large Animal Surgery Department of Large Animal Medicine College of Veterinary Medicine University of Georgia Athens, Georgia

Alan J. Ruggles, DVM, DACVS

Richard J. Piercy, MA, VetMB, MS, PhD, DACVIM, MRCVS

Allen M. Schoen, MS, DVM

Senior Lecturer in Equine Medicine and Neurology Veterinary Clinical Sciences Royal Veterinary College London, United Kingdom

Allen M. Schoen, DVM & Associates, LLC Sherman, Connecticut Director/Founder Veterinary Institute for Therapeutic Alternatives (VITA) Sherman, Connecticut

Robert C. Pilsworth, MA, VetMB, BSc, CertVR, MRCVS

Michael C. Schramme, DVM, CertEO, DECVS, PhD

Associate Newmarket Equine Hospital Newmarket Suffolk, United Kingdom Associate Lecturer Equine Hospital The Queen’s School of Veterinary Medicine Cambridge Cambridgeshire, United Kingdom

Partner, Staff Surgeon Department of Surgery Rood and Riddle Equine Hospital Lexington, Kentucky

Associate Professor, Equine Surgery Department of Clinical Sciences North Carolina State University Raleigh, North Carolina

Robert Sigafoos, CJF/Farrier Program/Planning Committee Kennett Square, Pennsylvania

Christopher C. Pollitt, BVSc, PhD

Roger K.W. Smith, MA, VetMB, PhD, DEO, DECVS, MRCVS

Honorary Professor of Equine Medicine School of Veterinary Science The University of Queensland Gatton Campus, Australia

Professor of Equine Orthopaedics Veterinary Clinical Sciences The Royal Veterinary College London, United Kingdom

Joanna Price, BSc, BVSc, PhD, MRCVS

Van E. Snow, DVM†

School of Veterinary Science University of Bristol Langford Bristol, United Kingdom

Sarah M. Puchalski, DVM, DACVR

Assistant Professor of Diagnostic Imaging Department of Surgical and Radiological Sciences University of California, Davis Davis, California

Norman W. Rantanen, DVM, MS, DACVR Fallbrook, California

Santa Ynez, California

Sharon J. Spier, DVM, PhD, Dipl ACVIM Professor Department of Medicine and Epidemiology School of Veterinary Medicine University of California Davis, California

Vivian S. Stacy, CNMT

Widener Hospital School of Veterinary Medicine University of Pennsylvania Kennett Square, Pennsylvania

†

Deceased.

Contributors

James C. Sternberg, DVM Powell Animal Hospital Powell, Tennessee

Anthony Stirk

Stirk & Associates Ltd. North Yorkshire, United Kingdom

Amanda Sutton, MSc Vet Phys. Chartered Physiotherapist Clinical Director Suttons Animal Physiotherapy Winchester Hampshire, United Kingdom

Alain P. Théon, DVM, MS, DACVR-RO Professor Department of Surgery and Radiology Oncology Service Chief Veterinary Medical Teaching Hospital School of Veterinary Medicine University of California, Davis Davis, California

Fabio Torre, DVM, DECVS, DAMS Director Clinica Equina Bagnarola Bagnarola, Bologna, Italy

Stephanie J. Valberg, DVM, PhD, DACVIM Professor Veterinary Population Medicine University of Minnesota College of Veterinary Medicine St. Paul, Minnesota

Robert Joseph Van Pelt, BVSc, BSc, CertEP, MRCVS Partner The Arundel Equine Hospital Arundel West Sussex, England

John P. Walmsley, MA, VetMB, Cert EO, DECVS, HonFRCVS The Liphook Equine Hospital Forest Mere, Liphook Hants, United Kingdom

Tim Watson, PhD, BSc, MCSP

Professor of Physiotherapy School of Health and Emergency Professions University of Hertfordshire Hertfordshire, United Kingdom

Renate Weller DMV, PhD, MRCVS, FHEA

Senior Lecturer in Veterinary Diagnostic Imaging Veterinary Clinical Sciences The Royal Veterinary College Hatfield, Hertfordshire, United Kingdom

R. Chris Whitton, BVSc, FACVSc, PhD Associate Professor Equine Centre University of Melbourne Werribee, Victoria, Australia

Jeffrey A. Williams, DVM Rhinebeck Equine LLP Rhinebeck, New York

Alan Wilson, BVSc, BVMS, PhD, MRCVS Professor Structure and Motion Laboratory Royal Veterinary College North Mymms, United Kingdom

Paul Wollenman, DVM

Palm Beach Equine Clinic, LLC Wellington, Florida

James Wood, BSc, BVetMed, MSc, MA, PhD, DipECVPH, DLSHTM Professor of Equine and Farm Animal Science Department of Veterinary Medicine University of Cambridge Cambridge, United Kingdom

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Foreword My first employer, the late Gordon Carter, and a man of real wisdom, once said to me: “You won’t know the meaning of ‘experience’ as a clinician until you have been in practice for 20 years, and then you will realise you don’t have any.” At the time I had no idea what he was talking about. I know now. The longer one is in practice, the less dogmatic and certain one often becomes. Horses accumulate, which just will not fit neatly into their diagnostic buckets. Prognoses, which were once certain fact, become turned on their heads by the horse that defies the clinician’s worst predictions, and comes back from injury against all the odds. Nerve blocks seem increasingly to eliminate pain from regions that were not their target, or do not abolish pain from areas that were. Radiography repeatedly shows no abnormalities in bones when magnetic resonance imaging (MRI) demonstrates gross and marked pathology. When meeting this plethora of square circles for the first time, the previously available textbooks just made one feel even more hopeless. Nerve blocks were either not needed at all for a diagnosis because a clinician of experience did not NEED to block a horse to know where the problem was. When it WAS employed, diagnostic analgesia eliminated pain in a totally predictable and specific way. All was black and white, clear cut, and specific. This was not the world of equine lameness that I was picking my way through as a novice clinician. Was I simply doing it wrong? Or was it perhaps that there are reasons why biological systems refuse to be pigeon-holed in the neat manner we would like them to be pigeon-holed? The first edition of Diagnosis and Management of Lameness in the Horse was a revelation in that respect. Here were clinicians determined to use a scientific and methodical approach to their horses, but at the same time describing all the many and varied ways that diagnostic tests could mislead. Moreover, here were clinicians who were even admitting to sometimes not making a diagnosis at all. The feeling of excitement one experienced in realising, as one read succeeding chapters, that other people were groping slowly forward in the same dark tunnel, with the same dim candles as one was oneself, was invigorating. Mike Ross and Sue Dyson redefined the equine lameness textbook in a way that was truly new, breathtaking in its breadth and depth of coverage, and for the first time addressing the fact that horses who perform in the many different disciplines we serve have many different clinical problems. Even horses with the same problems may be managed differently. For the first time each of our specialities was addressed in a clinically relevant manner, often by people at the height of their clinical powers. Although no substitute for experience itself, this massive accumulation of wisdom was put into the public domain, available to novice and expert alike. The very title uses the word

“management,” acknowledging that although we cannot always expect a total cure with treatment, the horse may be useful or may compete with careful management nonetheless. Isaac Newton once said “If I have seen a little further than others, it is only because I have stood upon the shoulders of giants.” We are in a golden age of equine diagnostic imaging, with ultrasonography, radiography, scintigraphy, computed tomography, and MRI all in frequent clinical use, allowing us to define with greater clarity the damage that produces the pain and therefore lameness in our patients. So who were those giants to whom we collectively owe so much? Many were mentioned in the Foreword to the first edition of this book, and some are omitted here solely through lack of space rather than respect. Ron Genovese and Norman Rantanen set up the field of ultrasonographic examination in the horse for us all to enjoy. In radiography, almost every useful paper in my formative years seemed to have the name Tim O’Brien on it somewhere. He, along with Bill Hornof and other colleagues at the University of Davis, California, United States described the oblique images of the third carpal bone, the flexed image of the distal aspect of the third metacarpal bone, and the “skyline” flexor surface image of the navicular bone, so valuable and yet now taken for granted. A single issue of Veterinary Clinics of North America devoted to Racetrack Practice published in 1990 advanced our knowledge vastly in the field of lameness in this field thanks to all of the authors, but from my own perspective, especially from the work of Roy Pool and Greg Ferraro, masters of their craft. Roy Pool was able to highlight the dramatic role that chronic, daily, repetitive microdamage played in the development of many “spontaneous” fractures. The days of the single misstep as the cause of the majority of fractures were becoming numbered, and even the acute carpal “chip” was shown to be anything but acute in most horses, certainly in terms of aetiology. I was fortunate in my early career to share a month “seeing practice” with Greg Ferraro, Tim O’Brien, and that pantheon of orthopaedics, Larry Bramlage, and that month altered the way I worked for the remainder of my career. There cannot be three people of greater wisdom, clinical skill, and willingness to share that expertise with others on the planet. As an equine orthopaedic surgeon also of great tact and humility (something of an oxymoron), Bramlage has also been a wonderful ambassador to our profession. He, along with Wayne McIlwraith, Dean Richardson, Ian Wright, and David Nunamaker, have added greatly to our knowledge of lameness from a surgical perspective. Scintigraphy was perhaps the biggest diagnostic leap forward for the racehorse, and has been useful in most other disciplines. This was only because of the dedication and willingness to share openly their knowledge with

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others by its founding fathers, and their able technicians. These include Gottlieb Ueltschi, Bob Twardock, Mike O’ Callaghan, and one of the editors of this book, Mike Ross, all giants indeed, to whom we should be grateful. In the field of MRI and diagnostic analgesia, the other editor of this book has made an enormous contribution. The name Sue Dyson has become a by-word for elegant, meticulous, probing studies by her and her team at the Animal Health Trust, Newmarket, England, carried out with great scientific integrity, documented in detail and published for all to share. She has made a unique and lasting contribution to studies of equine lameness, and the interlocking problems of the atypical consequences of the use of diagnostic analgesia, without in any way diminishing their importance as the foundation stone of lameness work—in fact, just the reverse. In MRI studies she joins other giants such as Russ Tucker and Rachel Murray who have opened up and explained this fascinating technique to the equine practitioner, and whose insights into the structural damage that leads to pain and consequently lameness have added so much to the various sections of this new edition. We must not forget the value of thorough clinical examination. The previous generation of lameness clinicians had no recourse to the advanced imaging modalities listed above, but they nevertheless diagnosed and treated horses, many of which returned to a useful life. We can argue that their presumptive diagnoses may have been incorrect in the light of what we know now, but they accumulated experience of which factors worked in restoring a horse with a specific set of clinical signs to soundness. Lameness practice, as pointed out in the first edition, is both an art and a science. The science is often dogma, a “best fit” for the current facts, but the art is a more continuous and constant tradition that many of the contributors to this second edition uphold and in turn pass on. An example of this would be pain which is abolished by both proximal palmar metacarpal (subcarpal) nerve blocks and later also by intraarticular analgesia of the middle carpal joint in a Thoroughbred racehorse. Many of these horses have slight thickening, possibly mild tenderness to palpation of the proximal suspensory ligament, and increased severity of lameness after carpal flexion, but no clinically significant lesion on ultrasonographic examination or radiography. For my generation, MRI is an available option, and in these circumstances one often finds a combination of injuries to the most proximal part of the suspensory ligament or its bone origin, the origin of the accessory ligament of the deep digital flexor tendon, the palmar carpal ligament, the interosseous ligaments between the third

and second and fourth metacarpal bones, or in areas of the third and radial carpal bones simply not visible radiologically. Ray Hopes, my mentor, previous employer, and now good friend, who founded the racing division of the Rossdale practice in Newmarket, England could not have recognised these injuries. Did he diagnose the condition of horses with the blocking history we have outlined? Yes he did. Did he treat these horses and successfully manage their return to training and competition? Very much so. He could not have known the true nature of the lesions. No-one in that era could have done so, but he accumulated enough wisdom and experience to know what one had to do, in terms of rest, therapy, and rehabilitation, to get those horses back to work, a legacy we still employ to the same end point today, possibly for different reasons and with more knowledge now of why it works. This second edition is not simply a reprint with minor changes to some sections. Every single chapter has been updated, some such as “The Tarsus” and “Navicular Disease” virtually rewritten; such is the avalanche of new knowledge that has come our way in the intervening 8 years. Almost all of the figures have been replaced with better quality digital images that significantly enhance the text. In addition some subjects not previously covered have now been included. Alan Wilson and Renate Weller contribute a new Chapter, “The Biomechanics of the Equine Limb and Its Effect on Lameness.” Whilst it may sometimes seem to us that all horses are lame, the majority of course are not. Careful study of biomechanics, particularly in the context of conformation and shoeing, may help us understand why one horse goes lame when its cohort group remains sound under the same exercise regimen. There are certain seminal textbooks that become so widely known, used, and respected in their field that the title of the book becomes subsumed by the name of the author in the public mind, as succeeding editions are updated and published. Sisson (anatomy), Lehninger (biochemistry), and Roitt (immunology) are books of this type. With this second edition, “Ross and Dyson” is about to join that list. It has become THE textbook on equine lameness. Clinicians certainly do not write textbooks with financial rewards in mind, or if they do, they have been wickedly deceived by their publishers! One has to hope that the knowledge that entire generations of equine practitioners will be enthralled, educated, and engaged by this masterly work will serve as just reward. Rob Pilsworth Newmarket, England January 2010

Second Foreword The production of veterinary texts addressing lameness in the horse has been very enlightening and, needless to say, a valuable tool to the equine practitioner. It is remarkable that the majority of the veterinary texts have been formulated within the past 50 years. Naturally, this incentive to produce texts has come from the resurgence of the number of horses in the United States. In the late 1920s, the number of horses in the United States was reported to be approximately 27 million. Dollar’s Veterinary Surgery was a text of note during this period, first being published in 1912; the second edition appeared in 1920, the third in 1937, and the fourth in 1950. In the Preface to the Fourth Edition, JJ O’Connor, MRCVS, who edited the third and fourth editions, made note of the nine additions of new material it contained. The last of the additions was “the examination of horses as to soundness” (approximately 200 pages). This time period is significant because the number of horses in the United States had dramatically dropped to approximately 750,000 by 1957. This precipitous drop in the number of horses prompted a general prediction that if the practice of equine veterinary medicine was not going to completely disappear, it would be a very limited part of veterinary medicine. Consequently, research into equine issues of note was very limited, if at all, and publications of scientific articles relevant to horses were also very limited. Basically no texts were produced after Dollar’s fourth edition until the early 1960s; however, in the 1950s a small number of devoted veterinarians, both practitioners and college professors, were diligent in pursuing the cause for the diagnosis and treatment of the lame horse. At the same time, there was a reversal in the decline of the number of horses in the United States. This stimulated more interest in equine veterinary medicine and spawned the resurgence of written material relevant to the lame horse. A reference point to this increase is the fact that the number of horses was reported to be 9.2 million (American Horse Council’s DeLoitte Report, June 5, 2005). Concurrently, the American Association of Equine Practitioners (AAEP) was born; this association has served since its inception as a medium to accumulate and disseminate information relevant to the lame horse. It was through the AAEP that I became familiar with the contribution by Dr. Mike Ross and Dr. Sue Dyson. In the first edition of Diagnosis and Management of Lameness in the Horse, in 2003, “Part I: Diagnosis of Lameness,” “Section 1: The Lameness Examination,” “Chapter 1, Lameness Examination: Historical Perspective,” Dr. Mike Ross states “in the mid to late 1900s Adams had the most profound influence by his teachings and writings.” He further references O.R. Adams’ 1957 “Veterinary Notes on Lameness and Shoeing of Horses” becoming the classic textbook, Lameness in Horses. As a graduate of Colorado State University in 1957, I consider it to be one of the

privileges of my veterinary career to have been a student of Adams, a part of his notes in 1957, and then a very close friend. Until Adams’ first edition of Lameness in Horses was published, his notes were invaluable to me. The historical perspective by Dr. Mike Ross echoes my thoughts regarding the assessment of the texts and information relevant to the study of the lame horse, including his reference to those that have influenced the molding of modern lameness detectives. An insight into the history of the printed material directed toward the diagnostic and therapeutic management of the lame horse allows a better insight into the appreciation of the modern printed texts relevant to this subject. Specifically the editors, in the first edition, presented the contents throughout the text in a very logical manner, providing excellent approaches to the resolution of the lame horse’s problems. The contents reflect the objective thinking of both editors and their contributors. The first nine chapters are vital to the lameness examination; the CD-ROM component enhances this segment in an extremely useful manner. When those principles are applied, then the logical application of the material in Chapters 10, 11, 12, 13, and 14 will follow as necessary. Paramount to lameness management is the identification of the pain site causing the lameness. When that has been accomplished, the direction to be taken to resolve the issue will be set. Certainly the material provided in Section 2 of Part I will be utilized as the next step in arriving at the specific site of the infirmity; however, when the factors described in Section 1 of Part I are carefully followed, resolution of the problem may not require the employment of diagnostic imaging. The approach outlined by Section 1 Part I serves as a reminder that the modern “lameness detectives” are provided with the faculties of observation, palpation, and a brain. When used properly, these will facilitate a diagnosis without the necessity of further diagnostic modalities; however, when necessary, diagnostic imaging is vital to the identification of the pain-producing lesions. Certainly the advancements in the diagnostic imaging modalities have enhanced our ability to arrive at a more precise diagnosis with the obvious benefit of arriving at a more complete treatment and prognosis. The second edition contains the revelation of more diagnostic detail than was available in the first edition. The editors have clearly provided a logical progression by structuring the contents of the text with the foot (Part II) following the general remarks regarding the diagnosis of lameness (Part I). Incorporation of recent discoveries of Robert Bowker, Christopher Pollitt, the editors, and others involved in studies of the foot will be useful information. The assessment of the information and input by the editors with their clinical experience should prove to make the understanding of the foot even more applicable to

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management of the information encountered in arguably the most common site of lameness in the horse. The flow of the text continues in a manner in which the diagnostician should proceed to arrive at an informed solution to the lameness problem. The incorporation of the axial skeleton (Part V) in the first edition continues to remind the equine practitioner that its evaluation is very much a part of the assessment of the lame horse. Certainly in my career the axial skeleton has gone from being of very little consideration to its importance today. The inclusion of recent approaches to the diagnosis of axial skeleton issues is going to be another welcomed event. The contributions to lameness other than those involving the skeleton and articulations as outlined in Parts VI, VII, and VIII of the first edition are updated as well. Certainly, there have been several new therapeutic modalities available for the management of lameness since the first edition. Again, the experience of the contributors and the editors will provide welcome information. Since publication of the first edition, the value of complementary therapy in equine practice continues to evolve, to demonstrate where it fits in Western medicine and the management of the lame horse. Part V, “Lameness in the Sport Horse” in the first edition provided valuable information into not only the differences between the types of lameness encountered in various

athletic endeavors of horses, but also those differences encountered throughout varying geographic locations. There is a difference in the degree of lameness from navicular disease and other soft tissue causes of palmar foot pain at 1609 meters compared with those at sea level. The CD-ROM component of the first edition has evolved into the website feature of the second edition. The 47 narrated videos of equine lameness provide not only insight into evaluating the more common types of lameness, but also provides examples of unusual cases that escape accurate description by the written word. I am confident that this second edition of Diagnosis and Management of Lameness in the Horse will be a major addition to the libraries of equine practitioners around the world. As a recipient of the contents of the texts that have been produced over the past years, I am extremely grateful and appreciative of the time and effort the editors, Mike W. Ross and Sue J. Dyson, and the contributors have put into this text. Not only does this information and the information provided by other similar literature aid the practitioner, but it has materially improved the health and welfare of the horses we care for. Marvin Beeman Littleton, Colorado, United States January 2010

Preface The second edition of Diagnosis and Management of Lameness in the Horse has been substantially revised. The knowledge that has been accrued through the clinical application of magnetic resonance imaging (MRI) and, to a lesser extent, computed tomography has revolutionized our understanding of many conditions, most especially those of foot pain. This is reflected by the greatly expanded section on the foot. In each chapter we have tried to reflect both our own advances in knowledge and those of our authors, as well as what has been published in the literature. Relevant new references are cited. We have introduced many new images, most acquired digitally and therefore of superior quality, but space constraints restrict what can be included. Some original illustrations reflecting unique conditions have been preserved. Some chapters have been written by different authors. This did not necessarily reflect that we were unhappy with the original authors, but rather that we wanted a different approach in some instances. We have again added editorial comments to some chapters when our personal experiences differed greatly from those of an author. As we work daily with lame horses our own knowledge and experience continue to grow. It is also inevitable that between submission of the material for the second edition to the publishers and the book’s publication, new literature has been published. Therefore although this new edition

reflects as far as possible state-of-the-art information, there are inevitably a few minor omissions. A major criticism of the first edition of the book was the quality of the binding. We were delighted to learn that the book was being used to such an extent that the bindings failed. We suspect that the second edition, being bigger, unfortunately may also suffer in the same way. We continue to learn by looking and seeing and encourage readers to watch the videos on the companion web site and listen to the commentaries, which we believe provide a fundamental background to the art of assessing a lame horse. We continue to hold the philosophy that a comprehensive clinical examination, combined with a logical approach to investigation, usually results in an accurate diagnosis, while acknowledging that a minority of horses elude diagnosis. There is a danger that with advances in imaging technology there is a temptation to utilize these tools excessively. We must remember that in many horses a correct diagnosis can be achieved by accurate palpation, observation, and use of diagnostic analgesia, combined with radiography and ultrasonography.

PREFACE—COMPANION WEB SITE

Although our views are similar in determining the end result of our examination during movement, we differ in our visual appraisal of the lame horse; for instance, Sue sees more vividly the downward movement of the pelvis when a horse with hindlimb pain causing lameness is in motion, whereas Mike sees the upward movement during a different portion of the stride. These differences and the different venues at which we complete our lameness examination are thoroughly explained in the narration. Examples are given of horses with unilateral and bilateral forelimb lameness, some with pain originating from common locations such as the foot or lower forelimb, while in others we contrast movement of these horses with those with pain emanating from the upper forelimb. Unilateral and bilateral hindlimb lameness is demonstrated and the concept of hindlimb lameness causing a head and neck nod—a situation during which a lameness diagnostician can confuse hindlimb with forelimb pain—is demonstrated in several video clips. The effect and use of circling a horse during lameness examination, a useful maneuver used to exacerbate lameness, is shown in horses with forelimb and hindlimb pain causing lameness. Concurrent forelimb and hindlimb lameness, the effect of a rider, and gait restriction as a result of thoracolumbar and sacroiliac

WWW.ROSSANDDYSON.COM When approached with the idea of developing the first edition of Diagnosis and Management of Lameness in the Horse we immediately determined that having video segments to accompany the text was a necessity, a way of providing moving figures to teach the fundamentals of the lameness examination during movement. At that time there were few textbooks with accompanying digital media and it was necessary to convert to digital format existing analog video footage. We then added newly acquired digital video segments to create the 47 individual files used in the CD-ROM that accompanied the first edition. It was not our intent to capture on video each and every nuance of the lame horse. We did, however, feel strongly in presenting the fundamentals of the lameness examination and the gaits and movement of the normal horse, and to contrast movement with the horses that have pain causing lameness, neurological abnormalities, mechanical deficits, and in brief esoteric gait disturbances. The art of the lameness examination during movement was captured.

Sue J. Dyson and Mike W. Ross Suffolk, United Kingdom and Pennsylvania, United States, December 2009

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region pain are demonstrated. Four horses with neurological gait abnormalities ranging from obvious to subtle, six horses with classic mechanical gait deficits causing lameness, and, finally, esoteric causes of gait abnormalities are shown. Listed below is the table of contents of the narrated video segments included in the web site accompanying the second edition of Ross and Dyson’s Diagnosis and Management of Lameness in the Horse. Using technological advances developed in the 8 years since the first edition was published we have changed the appearance of the media and improved its efficiency and utility. We have chosen to retain the original video segments and narration, feeling strongly that we have captured the essence of the lameness examination during movement and demonstrated the numerous principles of the lame horse. We debated endlessly whether to expand and include many more examples, to discuss flexion tests, to describe responses to local analgesic techniques and all the associated nuances, and to describe the many different clinical manifestations of pain arising from specific areas. Ultimately we decided not to, but we encourage readers to think about their own experiences and to share these with others. The video segments, moving figures, have been numbered from 1 to 47, and in the right margin of the text, when appropriate, we have printed an icon

referring

the reader to one or more of the video segments included in the accompanying web site we feel will be helpful to visually evaluate a horse during movement.

TABLE OF CONTENTS OF COMPANION WEBSITE Normal Gait

1. Gait of a normal horse when evaluated in-hand and while lunged 2. Gait of a normal horse while ridden

Unilateral Forelimb Lameness

3. Left forelimb lameness 4. Right forelimb lameness 5. Unilateral forelimb lameness resulting from upper limb pain 6. Unilateral forelimb lameness resulting from upper limb pain

Bilateral Forelimb Lameness

7. Bilateral forelimb lameness worse in the right forelimb

Effect of Circling on Forelimb Lameness

8. Right forelimb lameness 9. Bilateral forelimb lameness 10. Characteristics of carpal region pain

Hindlimb Lameness without a Head and Neck Nod

11. Left hindlimb lameness in a horse with stifle pain 12. Left hindlimb lameness in a horse with bilateral suspensory desmitis 13. Right hindlimb lameness in a horse with peritarsal soft-tissue injury 14. Right hindlimb lameness 15. Left hindlimb lameness, effect of the pace and trot during lameness examination

Hindlimb Lameness with an Associated Head and Neck Nod

16. Severe right hindlimb lameness from pain associated with fracture of the central tarsal bone 17. Severe left hindlimb lameness 18. Right hindlimb lameness as a result of severe osteoarthritis of the medial femorotibial joint 19. Severe left hindlimb lameness

Bilateral Hindlimb Lameness

20. Bilateral hindlimb lameness and plaiting while trotting 21. Bilateral hindlimb lameness exhibited as a reluctance to work

Effect of Circling on Hindlimb Lameness

22. Right hindlimb lameness and toe drag 23. Toe dragging while circling 24. Right hindlimb lameness worse going to the right

Concurrent Forelimb and Hindlimb Lameness

25. Left forelimb and left hindlimb lameness 26. Left forelimb and left hindlimb lameness in a Standardbred racehorse 27. Left hindlimb and right forelimb lameness causing a “rocking-type” gait 28. Left hindlimb and right forelimb lameness in a trotter before and after low plantar diagnostic analgesia 29. Bilateral hindlimb and mild forelimb lameness in a Thoroughbred racehorse with mal- or nonadaptive subchondral bone remodeling

Other Aspects of Hindlimb Lameness

30. Hindlimb lameness while ridden 31. Gait restriction from thoracolumbar pain 32. Gait restriction from sacroiliac region pain

Neurological Gait Deficits

33. Gait deficit in a horse with a cervical spinal cord lesion 34. Hindlimb ataxia and right shoulder instability 35. Hindlimb weakness 36. Gait deficit in a horse with cervical stenotic myelopathy

Mechanical Gait Deficits

37. Fibrotic myopathy 38. Stringhalt 39. Shivers 40. Upward fixation of the patella 41. Fibularis (peroneus) tertius injury in a mature horse 42. Fibularis tertius avulsion injury in a foal

Esoteric Gait Abnormalities

43. Right hindlimb gait abnormality 44. Running type of hindlimb gait 45. Aortoiliac thrombosis 46. Left hindlimb lameness and gait deficit in a horse with gastrocnemius origin injury 47. Idiopathic shortening of the cranial phase of the stride in a right hindlimb Mike W. Ross Sue J. Dyson December 18, 2009

Preface The second edition of Diagnosis and Management of Lameness in the Horse has been substantially revised. The knowledge that has been accrued through the clinical application of magnetic resonance imaging (MRI) and, to a lesser extent, computed tomography has revolutionized our understanding of many conditions, most especially those of foot pain. This is reflected by the greatly expanded section on the foot. In each chapter we have tried to reflect both our own advances in knowledge and those of our authors, as well as what has been published in the literature. Relevant new references are cited. We have introduced many new images, most acquired digitally and therefore of superior quality, but space constraints restrict what can be included. Some original illustrations reflecting unique conditions have been preserved. Some chapters have been written by different authors. This did not necessarily reflect that we were unhappy with the original authors, but rather that we wanted a different approach in some instances. We have again added editorial comments to some chapters when our personal experiences differed greatly from those of an author. As we work daily with lame horses our own knowledge and experience continue to grow. It is also inevitable that between submission of the material for the second edition to the publishers and the book’s publication, new literature has been published. Therefore although this new edition

reflects as far as possible state-of-the-art information, there are inevitably a few minor omissions. A major criticism of the first edition of the book was the quality of the binding. We were delighted to learn that the book was being used to such an extent that the bindings failed. We suspect that the second edition, being bigger, unfortunately may also suffer in the same way. We continue to learn by looking and seeing and encourage readers to watch the videos on the companion web site and listen to the commentaries, which we believe provide a fundamental background to the art of assessing a lame horse. We continue to hold the philosophy that a comprehensive clinical examination, combined with a logical approach to investigation, usually results in an accurate diagnosis, while acknowledging that a minority of horses elude diagnosis. There is a danger that with advances in imaging technology there is a temptation to utilize these tools excessively. We must remember that in many horses a correct diagnosis can be achieved by accurate palpation, observation, and use of diagnostic analgesia, combined with radiography and ultrasonography.

PREFACE—COMPANION WEB SITE

Although our views are similar in determining the end result of our examination during movement, we differ in our visual appraisal of the lame horse; for instance, Sue sees more vividly the downward movement of the pelvis when a horse with hindlimb pain causing lameness is in motion, whereas Mike sees the upward movement during a different portion of the stride. These differences and the different venues at which we complete our lameness examination are thoroughly explained in the narration. Examples are given of horses with unilateral and bilateral forelimb lameness, some with pain originating from common locations such as the foot or lower forelimb, while in others we contrast movement of these horses with those with pain emanating from the upper forelimb. Unilateral and bilateral hindlimb lameness is demonstrated and the concept of hindlimb lameness causing a head and neck nod—a situation during which a lameness diagnostician can confuse hindlimb with forelimb pain—is demonstrated in several video clips. The effect and use of circling a horse during lameness examination, a useful maneuver used to exacerbate lameness, is shown in horses with forelimb and hindlimb pain causing lameness. Concurrent forelimb and hindlimb lameness, the effect of a rider, and gait restriction as a result of thoracolumbar and sacroiliac

WWW.ROSSANDDYSON.COM When approached with the idea of developing the first edition of Diagnosis and Management of Lameness in the Horse we immediately determined that having video segments to accompany the text was a necessity, a way of providing moving figures to teach the fundamentals of the lameness examination during movement. At that time there were few textbooks with accompanying digital media and it was necessary to convert to digital format existing analog video footage. We then added newly acquired digital video segments to create the 47 individual files used in the CD-ROM that accompanied the first edition. It was not our intent to capture on video each and every nuance of the lame horse. We did, however, feel strongly in presenting the fundamentals of the lameness examination and the gaits and movement of the normal horse, and to contrast movement with the horses that have pain causing lameness, neurological abnormalities, mechanical deficits, and in brief esoteric gait disturbances. The art of the lameness examination during movement was captured.

Sue J. Dyson and Mike W. Ross Suffolk, United Kingdom and Pennsylvania, United States, December 2009

xv

xvi

Preface

region pain are demonstrated. Four horses with neurological gait abnormalities ranging from obvious to subtle, six horses with classic mechanical gait deficits causing lameness, and, finally, esoteric causes of gait abnormalities are shown. Listed below is the table of contents of the narrated video segments included in the web site accompanying the second edition of Ross and Dyson’s Diagnosis and Management of Lameness in the Horse. Using technological advances developed in the 8 years since the first edition was published we have changed the appearance of the media and improved its efficiency and utility. We have chosen to retain the original video segments and narration, feeling strongly that we have captured the essence of the lameness examination during movement and demonstrated the numerous principles of the lame horse. We debated endlessly whether to expand and include many more examples, to discuss flexion tests, to describe responses to local analgesic techniques and all the associated nuances, and to describe the many different clinical manifestations of pain arising from specific areas. Ultimately we decided not to, but we encourage readers to think about their own experiences and to share these with others. The video segments, moving figures, have been numbered from 1 to 47, and in the right margin of the text, when appropriate, we have printed an icon

referring

the reader to one or more of the video segments included in the accompanying web site we feel will be helpful to visually evaluate a horse during movement.

TABLE OF CONTENTS OF COMPANION WEBSITE Normal Gait

1. Gait of a normal horse when evaluated in-hand and while lunged 2. Gait of a normal horse while ridden

Unilateral Forelimb Lameness

3. Left forelimb lameness 4. Right forelimb lameness 5. Unilateral forelimb lameness resulting from upper limb pain 6. Unilateral forelimb lameness resulting from upper limb pain

Bilateral Forelimb Lameness

7. Bilateral forelimb lameness worse in the right forelimb

Effect of Circling on Forelimb Lameness

8. Right forelimb lameness 9. Bilateral forelimb lameness 10. Characteristics of carpal region pain

Hindlimb Lameness without a Head and Neck Nod

11. Left hindlimb lameness in a horse with stifle pain 12. Left hindlimb lameness in a horse with bilateral suspensory desmitis 13. Right hindlimb lameness in a horse with peritarsal soft-tissue injury 14. Right hindlimb lameness 15. Left hindlimb lameness, effect of the pace and trot during lameness examination

Hindlimb Lameness with an Associated Head and Neck Nod

16. Severe right hindlimb lameness from pain associated with fracture of the central tarsal bone 17. Severe left hindlimb lameness 18. Right hindlimb lameness as a result of severe osteoarthritis of the medial femorotibial joint 19. Severe left hindlimb lameness

Bilateral Hindlimb Lameness

20. Bilateral hindlimb lameness and plaiting while trotting 21. Bilateral hindlimb lameness exhibited as a reluctance to work

Effect of Circling on Hindlimb Lameness

22. Right hindlimb lameness and toe drag 23. Toe dragging while circling 24. Right hindlimb lameness worse going to the right

Concurrent Forelimb and Hindlimb Lameness

25. Left forelimb and left hindlimb lameness 26. Left forelimb and left hindlimb lameness in a Standardbred racehorse 27. Left hindlimb and right forelimb lameness causing a “rocking-type” gait 28. Left hindlimb and right forelimb lameness in a trotter before and after low plantar diagnostic analgesia 29. Bilateral hindlimb and mild forelimb lameness in a Thoroughbred racehorse with mal- or nonadaptive subchondral bone remodeling

Other Aspects of Hindlimb Lameness

30. Hindlimb lameness while ridden 31. Gait restriction from thoracolumbar pain 32. Gait restriction from sacroiliac region pain

Neurological Gait Deficits

33. Gait deficit in a horse with a cervical spinal cord lesion 34. Hindlimb ataxia and right shoulder instability 35. Hindlimb weakness 36. Gait deficit in a horse with cervical stenotic myelopathy

Mechanical Gait Deficits

37. Fibrotic myopathy 38. Stringhalt 39. Shivers 40. Upward fixation of the patella 41. Fibularis (peroneus) tertius injury in a mature horse 42. Fibularis tertius avulsion injury in a foal

Esoteric Gait Abnormalities

43. Right hindlimb gait abnormality 44. Running type of hindlimb gait 45. Aortoiliac thrombosis 46. Left hindlimb lameness and gait deficit in a horse with gastrocnemius origin injury 47. Idiopathic shortening of the cranial phase of the stride in a right hindlimb Mike W. Ross Sue J. Dyson December 18, 2009

PART I

Diagnosis of Lameness SECTION 1

The Lameness Examination Chapter

1 

Lameness Examination: Historical Perspective Mike W. Ross

References on page 1255

If your horse is lame in his shoulder, take off his shoes.… Young and inexperienced practitioners are quite too apt to commit the error of overlooking the examination of the foot, looking upon it as a matter of secondary importance, and attending to it as a routine and formal affair only. A. Liautard, 18881

As the twenty-first century continues, the extent of change in the diagnosis of lameness in the horse depends on the individual’s clinical and ideological perspective. A veritable explosion of new imaging methods such as digital radiography, computed tomography, and magnetic resonance imaging has advanced the current understanding of many musculoskeletal abnormalities. Yet to accurately assess clinical relevance, the clinician must possess a feel for the horse, developed only by careful clinical examination, a procedure that has changed little in hundreds of years. Successful detection of equine lameness does not so much require knowledge of science as it does art. Inasmuch as art is defined as “skilled workmanship, craft, or studied action,”2 the lameness examination demands artistic experience acquired by years of clinical practice and working and learning from experienced practitioners. From Liautard’s advice more than 100 years ago to that of modern lameness diagnosticians, the change in the basic skills of lameness diagnosis may be small. Development of the artistic skills needed to become a true lameness diagnostician requires a thorough, somewhat methodical approach, much like that of a crime scene detective. I often refer to the lameness diagnostician as a lameness detective, and although this statement may lack sophistication, in reality, how boring would the task be if the horse could talk? To make a horse talk to you through careful palpation and observation is the essence of the

lameness examination, yet most difficult to teach. Great lameness diagnosticians likely possess this ability to read or feel the horse and skilled, workmanship-like qualities to appreciate the art in lameness diagnosis. Some, with the added ability to share this knowledge effectively, have influenced clinicians more than others simply by writing about those experiences. In the early twenty-first century, Ross and Dyson’s Diagnosis and Management of Lameness in the Horse chronicled the exhaustive clinical experience of over 100 authors worldwide to capture the essence of the subject at that time.3 Moving figures captured as video segments on an accompanying CD and individual chapters detailing lameness distribution among different sporting activities complemented basic and advanced material.3 The book quickly became a staple of every lameness diagnostician’s library. In the mid-tolate 1900s, Adams had the most profound influence with his teachings and writings. His former students and friends acknowledge his artistic talent, gained primarily from a ground-up approach to the lame horse, and his profound interest in corrective shoeing. More important, Adams’ original lameness notes became his classic textbook.4 For most clinicians, Lameness in Horses represented the “lameness Bible,” an excellent resource of information on equine lameness. Adams himself revised the textbook several times; most recently, his respected colleague, Ted S. Stashak, has continued in Adams’ footsteps. This important work served as the foundation for learning the fundamentals of equine lameness for many during this period. Adams was influenced greatly by the work of Dollar and Lacroix. Adams’ original notes contain many drawings similar to those originally published in Dollar’s A Handbook of Horseshoeing,5 a wonderful collection of drawings and excellent descriptions of shoeing, conformation, and lameness of the equine foot. Adams references the work of Lacroix6 in the late 1800s. In fact, until Adams’ treatise on lameness, scant information about equine lameness existed. The information available in the American literature during most of the 1900s consisted of only sporadic case reports or case series in the Journal of the American Veterinary Medical Association. A potential explanation may lie in the importance of the World Wars or other important social events in the early-to-mid 1900s. Experience in the cavalry also may have influenced later writings in the 1900s.

1

2

PART I  Diagnosis of Lameness

Peters’7 work detailing lameness in the Thoroughbred racehorse emphasized the importance of lameness in the racetrack practice and the most common cause of poor performance. Many problems he observed in 1939 still exist, although treatment options have expanded considerably. Early important writings included manuscripts by Churchill8 and Wheat and Rhode9 on surgical removal of proximal sesamoid bone fractures (the Churchill approach), Forsell10 on surgical management of navicular bursitis and tendonitis, and Lundvall11 and later Delahanty12 debating the subject of the existence or nonexistence of fibular fractures. An early reference of note was the surgical textbook by Frank.13 Originally written in 1939, with several subsequent editions, this influential and often quoted textbook contained information about numerous musculoskeletal problems and often sensational examples of common and rare abnormalities. In the late 1800s, several informative, interesting, and entertaining textbooks about equine lameness were written, primarily by European authors. Most publications contained wonderful descriptions of lame horses, and many emphasized shoeing techniques, a mainstay in management of the lame horse both then and now. The writings of Percivall14 and Gamgee15 are particularly informative. Although a definitive reason was not provided, Gamgee observed that 42% of horses in the United Kingdom were lame, whereas only 9% of horses in Paris were lame. Disorders of the foot, many of which increased in frequency with age, were most common, and marked remodeling of the distal phalanx was seen in horses undergoing postmortem examination.15 In addition to the time-honored management technique of shoeing the lame horse, conformation and its relationship to lameness also were emphasized. In How to Judge a Horse, Bach16 emphasized balance, body part length and angulation, and distal extremity conformational faults. In modern day lameness examinations, conformation and its role in the development of lameness are often given cursory emphasis but remain an important part in the art of the examinations. In a chapter entitled “Horse-Docturing [sic] in the Nineteenth Century,” Dunlop and Williams17 emphasized the contribution of Mayhew, described as artist, activist, and veterinary surgeon. Mayhew described and illustrated many common abnormalities of the locomotor system recognized at that time, including splints, spavin, curb, tendon sprains, and thoroughpin, most of which are still recognized today.17 Of interest, Mayhew was credited for trying “experimental” injections into inflamed areas, an obviously important treatment modality practiced today.17 Detailed descriptions of laminitis, navicular disease, and other common conditions of the equine foot were provided.17 Dunlop and Williams,17 in their treatise on the history of veterinary medicine, also detailed the transition from farriery to veterinary medicine that occurred in the 1700s, although the close association and harmonious working relationships between blacksmiths and equine

diagnosticians remain integral parts of a successful lameness management team today. In fact, “the term veterinarian came into use when colleges were established in different parts of Europe for improving, or rather for creating the art of treating disease in the lower animals.”17 The first veterinary school was founded in France in 1761, and soon veterinary schools were formed in the United Kingdom.18 Although an exhaustive historical review might be interesting, this brief review highlights critical issues central to modern lameness diagnosis. First, the basics have not changed for hundreds of years and will likely not change in the foreseeable future. Second, with the exception of Adams’ work, and more recently that of Ross and Dyson, few comprehensive reports on lameness diagnosis were written before the twenty-first century. The modern lameness detective likely has learned most from experience working with accomplished lameness diagnosticians and by word of mouth. Third, many of our most knowledgeable colleagues have not published writings but have made their contributions in day-to-day teachings in academic settings, private practice, and small gatherings at national meetings. Since 1955 the annual convention of the American Association of Equine Practitioners has played a special role in the dissemination of information and ideas about lameness. Early meetings included a handful of practitioners, gathering and discussing equine medicine and surgery, sometimes late into the night. Much current lameness experience can be traced to these early meetings and practitioners such as Adams, Peters, Frank, Farquharson, Churchill, Goddall, Gabel, and Delahanty. Loren Evans and Howard “Gene” Gill influenced the molding of many modern lameness detectives, including me. Emphasizing the value of acquiring horse sense and spending time palpating and “learning” the horse, Gill often quotes Will Rogers, “… the outside of a horse is good for the inside of a man.” In the United Kingdom the British Equine Veterinary Association was established in 1961, providing a similar formula for dissemination of information through its annual congress and regular day meetings. The establishment of the Equine Veterinary Journal in 1968 provided a high-quality, refereed journal. The standard for the journal was set by the first editor, John Hickman, an astute observer of lame horses and an influence on many practitioners. No substitute exists for careful clinical examination and observation, experience gained over many years of treating and developing a feel for the lame horse. The second edition of this textbook on lameness is once again a collection of the best and most knowledgeable lameness diagnosticians worldwide. Some are “household lameness names,” whereas others are less renowned. All have one thing in common: they practice the art of lameness diagnosis and management in the horse.

Chapter 2  Lameness in Horses: Basic Facts Before Starting



Chapter

2 

Lameness in Horses:   Basic Facts Before Starting Mike W. Ross

3

with diagnostic analgesia is a prudent choice. Trial and error also occasionally work and in some instances may be the preferred approach. Intraarticular analgesia can be performed in selected joints without disrupting distal-toproximal perineural techniques later during the same examination. However, because pathognomonic signs are rare, proficiency in diagnostic analgesic techniques is mandatory for the lameness diagnostician.

BASELINE AND INDUCED LAMENESS

References on page 1255

The clinical manifestations of lameness in the horse are well known, but an exact definition is difficult. The word lame is an adjective, meaning “crippled or physically disabled, as a person or animal … in the foot or leg so as to limp or walk with difficulty.”2 A medical dictionary defines lameness as “incapable of normal locomotion, deviation from the normal gait.”3 The noun lameness can be, but infrequently is, used interchangeably with claudication, described as “limping or lameness.”3 Lameness is simply a clinical sign—a manifestation of the signs of inflammation, including pain, or a mechanical defect—that results in a gait abnormality characterized by limping. The definition is simple, but recognition, localization, characterization, and management are complex.

Baseline, or primary, lameness is the gait abnormality recognized when the horse is examined at a walk or trot in hand before flexion or manipulative tests are used. The clinician usually recognizes this abnormality by watching the horse on a firm or hard surface, while it is being trotted in a straight line. Diagnostic analgesia is used to abolish this lameness. Changing the surface or nature of the exercise by lunging, or circling the horse at a trot in hand, potentially changes the baseline lameness. The surface and exercise (gait and speed) must be consistent. In some horses no observable lameness is present at a walk or trot in hand. Lameness may be evident when the horse is ridden, and this lameness becomes the baseline lameness. Flexion tests and other forms of manipulation are used to exacerbate baseline lameness or to induce lameness. An induced lameness is one that is observed after flexion or manipulative tests, but induced lameness may not be the same as the baseline lameness. Manipulative tests are expected to, and often do, exacerbate the primary lameness. However, flexion and manipulative tests can cause development of additional lameness, unrelated to the primary or baseline lameness, and test results must be interpreted carefully.

LOCALIZATION OF PAIN

COEXISTENT LAMENESS

In certain conditions, characteristic gait abnormalities allow immediate and straightforward recognition and localization of the problem. Sweeny, fibrotic myopathy, upward fixation of the patella, stringhalt, shivers, and radial nerve paresis are examples. However, similar gait deficits exist for a variety of lameness problems, complicating recognition and localization. A fundamental concept in lameness diagnosis is the application of diagnostic analgesic techniques to localize the source of pain causing lameness. The sequence of properly determining the lame leg (recognition) and then abolishing the clinical sign of lameness by use of diagnostic analgesia (localization), only to have lameness return when the local anesthetic effects abate, is essential for accurate diagnosis. In essence diagnostic analgesia establishes clinical relevance, a most important concept to the lameness diagnostician. With experience and under certain circumstances, this step in lameness diagnosis can be omitted. The degree of lameness, certain gait characteristics, and palpation findings allow the clinician to strongly suspect a certain diagnosis. The next step may be diagnostic imaging. For example, a racehorse with prominent lameness after training may be suspected of having a stress or incomplete fracture. Performing radiographic and scintigraphic examinations before proceeding

Horses often have several sites of pain, although one usually is most obvious and the cause of baseline lameness. In many horses, secondary or compensatory (sometimes referred to as complementary) lameness develops in predictable sites or limbs. Concomitant bilateral forelimb or hindlimb lameness is common, but horses often demonstrate more prominent clinical signs in one limb. In horses with palmar foot pain, initially pronounced single forelimb lameness that is abolished by palmar digital analgesia may be present, with subsequent recognition of contralateral forelimb lameness. In racehorses, bilateral lameness, such as in the carpi or metacarpophalangeal or metatarsophalangeal joints, is common. The clinician should carefully examine the contralateral limb. Predictable compensatory or secondary lameness often exists in the ipsilateral or contralateral forelimb when primary lameness is present in the hindlimb, or vice versa. In a Thoroughbred (TB) racehorse with left forelimb lameness, compensatory problems in the right forelimb and left hindlimb are not uncommon, because these limbs presumably are succumbing to excessive loads while protecting the primary source of pain. In a trotter, diagonal lameness often occurs (primary lameness in the left hindlimb and compensatory lameness in the right forelimb), whereas in pacers, ipsilateral lameness is

Lameness is therefore not so much an original evil, a disease per se, as it is a symptom and manifestation of some antecedent vital physical lesion, either isolated or complicated, affecting one or several parts of the locomotive apparatus. A. Liautard, 18881

DEFINITION

4

PART I  Diagnosis of Lameness

most common (primary right forelimb and compensatory right hindlimb). When several limbs are involved, identifi­ cation of the primary or major source of pain is important. If forelimb and hindlimb lameness exist simultaneously, diagnostic analgesic techniques should begin in the hindlimb (see Chapter 10). A common secondary lameness abnormality, proximal suspensory desmitis, can develop in the compensating forelimb or hindlimb. Coexistent lameness can make assigning primary or baseline lameness to a particular limb during lameness examination difficult (see Chapter 7). Bilaterally symmetrical pain may cause a short, choppy gait, but primary or baseline lameness often cannot be seen when the horse is examined in a straight line in hand. Often, horses with coexistent lameness must be circled, lunged, or ridden for primary or baseline lameness to be observed. The lameness diagnostician may have to arbitrarily assign lameness to a limb and begin diagnostic analgesia in this manner. Often, once the primary source of pain has been identified, horses show pronounced lameness of much greater magnitude than expected in another limb, vivid clinical evidence that coexistent lameness exists.

LAMENESS DISTRIBUTION Among all types of horses, forelimb lameness is more common than hindlimb lameness. A horse’s center of gravity or balance, while dictated to a certain extent by conformation (see Chapter 4), is not located in the center

of the horse but is closer to the forelimbs than the hindlimbs. Thus the forelimb/hindlimb (F/H) weight (load) distribution ratio is approximately 60% : 40% (Figure 2-1). Higher loads are expected on the individual forelimbs (30% each), predisposing the horse to greater injury. At certain times during the stride cycle of gaits such as the canter (three-beat gait) and gallop (four-beat gait), a single forelimb is weight bearing, which predisposes the limb to injury. The weight of a rider may shift F/H load distribution to 70% : 30% (Figure 2-2). Two-beat gaits, such as the pace and trot, allow more equal load sharing between forelimbs and hindlimbs because a forelimb and hindlimb (ideally, if the gait is balanced perfectly) hit the ground simultaneously. In pacers and trotters the proportion of forelimb lameness is less than in the TB racehorse. The added load of pulling a sulky, cart, or any heavy load increases the likelihood of hindlimb lameness in Standardbreds (STBs), other harness breeds, and draft horses (Figure 2-3). The F/H distribution of lameness in STB racehorses is 55% : 45%. Sporting activities such as dressage and jumping also may shift lameness distribution to the hindlimbs because collection (working off the hindlimbs) and propulsion needed by horses to perform these activities may predispose to hindlimb lameness. The tendency of good moving dressage horses to show advanced diagonal placement in trot results in a single hindlimb bearing weight. In the forelimb, up to 95% of lameness problems occur at the level of or distal to the carpus.4 The distal parts of the limb always should be excluded as a potential source

Center of balance Fig. 2-1  •  The center of balance (gravity) of the horse is located closer to the forelimbs, which accounts for the load distribution difference between the forelimbs and hindlimbs. Conformation, namely the angles of the shoulder and rump, and weight of the head and neck and gait can change this load distribution.

Chapter 2  Lameness in Horses: Basic Facts Before Starting



5

WEIGHT

Cranial shift in center of balance Fig. 2-2  •  Gaits such as the canter and gallop (depicted) and the added weight of a rider, as shown here in a Thoroughbred racehorse, increase load on the forelimbs by shifting the center of balance, thus increasing the likelihood of forelimb lameness.

of lameness before the upper limb is addressed, although many owners believe otherwise and may try to mislead an inexperienced practitioner. The foot should be suspected first. Pain in the foot is one of the most common causes of forelimb lameness in all types of horses, and in draft breed horses, the foot is also the most common site of pain in the hindlimb.

Hindlimb Lameness

Hindlimb lameness should not be underplayed, although its recognition is more difficult. In the forelimb lameness– prone TB racehorse, many hindlimb lameness problems are overlooked. However, a rider or jockey often may suspect a hindlimb problem when the lameness actually exists in the forelimb. A practitioner should consider carefully the distribution of sites of hindlimb lameness. Historically, the hock has been regarded as the major source of problems, and although it is an important source of hindlimb lameness, other sites also are important. For instance, in both the TB and STB racehorse the metatarsophalangeal joint is a major source of lameness that historically has been overlooked.5,6 Maladaptive or nonadaptive bone remodeling of the distal aspect of the third metatarsal bone cannot be seen

radiologically in early stages and requires careful diagnostic analgesic techniques to achieve localization. Scintigraphic examination is mandatory for definitive diagnosis.7 Lameness of the metatarsophalangeal joint in STBs is almost as common as that of the hock, but without careful examination and the use of diagnostic analgesia, hock lameness is suspected in many such horses and they are treated for it. In sports horses proximal suspensory desmitis is now recognized as a more important cause of lameness than hock pain. The combined use of diagnostic analgesia, ultrasonography, and scintigraphy has increased clinical knowledge of the broad spectrum of lameness conditions in the hindlimbs. In the draft horse, lameness in the hindlimb most commonly develops in the foot. Lameness in this area reflects the work performed by these horses, and innate characteristics of the draft horse foot, which predispose the foot to conditions such as laminitis. In jumping and dressage horses, problems in the fetlock region such as osteoarthritis and tenosynovitis are common and reflect the stress imposed by these disciplines. Although owners, trainers, and veterinarians often suspect an upper hindlimb lameness, gait characteristics of lower limb lameness problems often are similar. Only use of diagnostic analgesia allows an accurate diagnosis.

6

PART I  Diagnosis of Lameness

WEIGHT

Caudal shift in center of balance Fig. 2-3  •  In a Standardbred racehorse (pacer depicted), the hindlimbs share added load compared with a Thoroughbred racehorse because of a caudal shift in the center of balance. The type of harness with the overcheck bit, the added weight of the sulky and driver, and the necessity of pulling a load increase the likelihood of hindlimb lameness in this breed.

RELATIONSHIP OF LAMENESS AND CONFORMATION Conformation of the distal extremities, and to a lesser extent the overall body, plays a major role in the development of forelimb and hindlimb lameness (see Chapter 4). When a practitioner examines a weanling or yearling with poor conformation, predicting the time and the exact way the lameness will occur may be difficult, but many well-recognized conformational faults can lead directly to lameness problems. Conformational faults of the carpus, such as carpus varus or valgus, back-at-the-knee, and offset knees, can be important factors in carpal and lower forelimb lameness. In the hindlimbs, excessively straight hindlimbs (“straight behind”) and sickle-hocked and in-atthe-hock conformation can lead directly to predictable lameness conditions. Although exceptions do exist, in the case of poor conformation, predictable lameness conditions consistently develop in poorly conformed horses. Evaluation of conformation is therefore an essential part of a lameness examination.

POOR PERFORMANCE Convincing trainers and owners may be difficult, but the leading cause of poor performance in racehorses is lameness, and lameness is the most prevalent health problem among all horses.8-11 In one study, 50% of North American

operations with three or more horses had one or more lame horses, and 5% of the horses could be expected to be lame.10 In another study, 74% of racehorses evaluated for poor racing performance had substantial musculoskeletal abnormalities contributing to poor performance. Lameness examination was emphasized as a most important aspect of comprehensive performance evaluation.12,13 Others have emphasized the importance of lameness in epidemiological studies evaluating wastage in TB racehorses.14,15 Recently, lameness was once again found to be the most important condition causing missed training days in TB racehorses training in the United Kingdom.16 Two-year-olds missed training days significantly more than 3-year-olds, and stress fractures were the most important cause of lameness.16 Disappointingly, there has been little change in the importance of lameness and missed training days in the United Kingdom over a 20-year period.16 The same is likely true among all sports horses, particularly those competing at upper levels, although comprehensive studies have not been performed. Obvious lameness need not be demonstrated for performance to be compromised in horses, especially those competing at high speeds or upper levels. The possibility of achieving maximal performance in horses with substantial lameness is a common misconception. I have examined numerous top-level STB and TB racehorses in which easily recognized lameness is seen when the horses are trotted in hand on a hard surface. Notwithstanding the ignorance of many in the horse industry, the ability



Chapter 2  Lameness in Horses: Basic Facts Before Starting

of many horses with obvious lameness to compete is a tribute to their mental and physical toughness. For example, bilateral forelimb or hindlimb lameness is common in racehorses but in some instances goes unrecognized if the condition is of similar severity in both limbs. Unilateral lameness of this magnitude would be recognized easily, but because the lameness is bilateral, horses still race, albeit at a lower level. Bilateral third carpal slab fractures and sagittal fractures of the proximal phalanx have been diagnosed in horses examined for poor racing performance but, if seen unilaterally, would have caused pronounced lameness. Part of the art of the lameness examination is separating those horses capable of performing with moderate pain at a high level from those that cannot do so.

GAIT DEFICITS NOT CAUSED BY LAMENESS Gait abnormalities can exist with or without the presence of clinically apparent lameness. Deficits such as stringhalt, mild intermittent upward fixation of the patella, and shivers (see Chapter 48) can be present without obvious lameness and may complicate diagnosis of a completely different primary source of pain causing lameness. Horses with neurological disease may have gait deficits that are considered the result of painful lameness conditions (see Chapter 11). Horses with lower motor neuron diseases, such as equine protozoal myelitis, may have lameness associated with muscle atrophy or unexplained low-grade lameness associated with the disease. Concomitant lameness conditions can and do occur in these horses. Recurrent exertional rhabdomyolysis can cause stiffness and in some instances lameness, or it can cause poor racing performance, all of which can be misinterpreted as lameness (see Chapter 83).

UNEXPLAINED LAMENESS A diagnosis is made for most, but not all, lame horses through careful clinical examination and ancillary imaging modalities. Even with advanced imaging techniques, a solution is not always found (see Chapter 12), but it is hoped that future innovations in clinical examination and imaging will result in the continued expansion of the science of lameness diagnosis.

COMPONENTS OF THE LAMENESS EXAMINATION AND LAMENESS STRATEGY Lameness Examination

Lameness examinations should be performed in an orderly, step-by-step way, but many factors may change or abbreviate the examination (Box 2-1). Owner financial constraints may not allow performance of certain diagnostic tests and may curtail the time necessary to complete the entire examination. Drug testing of competing racehorses or show horses may limit a practitioner’s ability to perform diagnostic analgesic techniques and restrict management options. Clients do not always understand the need for diagnostic analgesia. Education about the value of this technique, and the difficulties of interpretation of the results of diagnostic imaging without it, is vital. Abbreviated lameness examinations often are performed in horses that exhibit severe lameness compatible with a

7

BOX 2-1 

Components of the Lameness Examination History—anamnesis Examination from a distance—conformation, symmetry, posture Palpation Hoof tester examination Physical examination—other ancillary testing Movement Baseline Additional movement Selected examinations—manipulation, flexion, direct pressure, wedge Diagnostic analgesia Imaging Diagnosis Certain, presumptive, open Management Follow-up examination

fracture. Typical or obvious clinical signs may accompany severe lameness, and in many instances prolonged or extensive lameness examination is contraindicated. If incomplete fractures are suspected, diagnostic analgesic techniques may be dangerous and should be performed only in certain situations. A clinician may proceed directly to conventional or advanced imaging techniques before completing the initial steps of a conventional lameness examination. Many other factors affect the ability to complete a comprehensive evaluation. Time constraints (usually of the veterinarian) often are cited, although shortcuts, if taken, usually create future problems. Omission of a diagnostic block or failure to perform detailed palpation often leads to misdiagnosis. Omission of a brief physical examination, including assessment of the horse’s temperature, can lead to embarrassing situations. The footing available on which to complete the lameness examination can be problematic. A dry, flat, hard surface or space for lunging or riding may be unavailable. The horse’s temperament may preclude adequate movement and often limits the practitioner’s ability to perform diagnostic analgesia. Many ill-tempered horses are referred for advanced imaging techniques, such as scintigraphic examination, because diagnostic analgesic techniques are dangerous to the veterinarian and handler.

Lameness Etiquette

Owners frequently request an opinion from more than one veterinarian. Therefore professional, ethical conduct is important, with practitioner acknowledgment that horses can appear very different every day and that response to diagnostic analgesia is not always consistent. For example, differences of opinion concerning radiological interpretation can exist. A good working relationship with the client or agent is essential but should extend also to the farrier and any paraprofessionals involved in the management of the horse, even when opinions differ.

Prognosis Assessment

Assessment of prognosis for performance is important, but because few published data relating to many sports disciplines are available, clinicians often must rely on

8

PART I  Diagnosis of Lameness

personal experience based on an understanding of the sport. Owners and trainers should consider prognosis carefully when making decisions to pursue therapeutic options, particularly when a long layoff period is required. I prefer to define prognosis as the “chance the horse will return to its previous level of competition.” However, this may not be a fair or reasonable definition. Retrospective studies can be used to evaluate prognosis after surgical or conservative management for various conditions in racehorses. Objective data such as numbers of race starts, race times, earnings per start, and time from treatment to first race start can be assessed. Earnings per start is an important criterion because it establishes racing class or level of competition. However, in most retrospective studies, earnings per start decrease after treatment. The question is whether practitioners can accurately state that the horse will drop in class after treatment and whether this drop in class is the result of the injury, treatment, or aging of the horse an additional year before returning to racing. Use of this information is not easy. Most owners and trainers have a different view of prognosis than the veterinarian. In considering the prognosis for a horse undergoing arthroscopic surgical removal of a small osteochondral fracture of the carpus, most owners emphasize the surgery rather than the original injury. Clinicians must explain thoroughly the magnitude of the injury and related damage and discuss prognosis, using terminology that clearly indicates that the extent of injury is the factor that determines prognosis. Expecting a racehorse to return to its previous racing class may be an unrealistic expectation or at least a very strict definition for success. In a retrospective study of postoperative racing performance of STBs treated for carpal chip fractures, 74% of horses made at least one race start after surgery.17 Median earnings per start significantly decreased, but the median race mark (best winning time)

also significantly decreased, indicating that horses made less money but raced faster after surgery.17 These results must be compared with a normal population of STBs as the horses age, without considering injury, because STB racing performance is not standard over time.18 Average earnings per start is highest in 2-year-old horses and decreases exponentially until retirement.18 A population of horses undergoing any long-term layoff that requires recommencement of racing the following year can be expected naturally (unrelated to the original injury) to have lower earnings per start, regardless of whether an injury occurred or treatment was given. Therefore retrospective studies may underestimate prognosis associated with injuries and management choices. Success criteria and outcome assessment must be standardized to compare treatment results and to define prognosis. The current standard for racehorses is comparison of performance for five starts before and after injury and treatment. This criterion is strict; a practitioner first may prefer to predict the chance of the horse returning to racing and then assess the chance that the horse will perform at or near its previous level. Other statistical methods have been used to evaluate racing performance in TBs using a regression model accounting for variables such as track surface, race distance, and age.19-21 To date, this performance analysis has been restricted to evaluation of horses after upper respiratory tract surgery but probably will be applied to horses with musculoskeletal injuries. When comparing published information regarding management of various types of lameness, the clinician should be clear about criteria for inclusion of cases and be sure to compare “apples to apples.” For instance, comparing results of management of horses with chronic, recurrent hindlimb suspensory desmitis to those with acute forelimb suspensory desmitis is unfair.

Chapter

3 

Anamnesis (History) Mike W. Ross The importance of a detailed clinical history, the anam­ nesis, cannot be overemphasized. Information is divided into two categories: basic facts necessary for every horse, and additional information from questions tailored to the specific horse. The veterinarian must understand the breed, use, and level of competition of each horse, because prognosis varies greatly among different types of sports horses. Firsthand experience of the particular type of sports horse being examined is useful but is not essential. Clinicians must understand the language associated with the particular sporting event, and this may be a challenge. For some sporting events, understanding the clinical history and having the ability to ask the right questions are like

speaking a different language. A veterinarian unfamiliar with the sporting activity should briefly review the type of activities performed and the array of potential lameness problems encountered with them (see Chapters 106 to 129). In some instances the veterinarian may lose credibility when talking to trainers or riders, particularly those involved in upper-level competition, if they perceive unfamiliarity. The veterinarian must understand the difference between subjective and objective information in the clinical history. Objective information is gained from the horse, and subjective information is perceived by the rider or owner. Knowledge about a horse’s performance such as “the horse is bearing out,” “the horse is on the right line,” “the horse is lugging in,” “the horse has just started to refuse fences,” or “the horse no longer takes the right lead” is valuable objective information. Common examples of information perceived by the owner or rider include “the horse feels off behind,” “the horse is stiff behind,” or “the horse is lame behind” and it “feels up high.” Such information generally is useful and indicates a change in the horse’s gait, but only an experienced rider or trainer

can discriminate accurately between forelimb and hindlimb lameness at any gait. Erroneous information obtained from the rider can complicate communication during lameness examination, particularly if the individual is strong-willed and seemingly authoritative; this situation occurs if riders or trainers insist they are correct and the veterinarian disagrees. In my experience, many horses considered to have hindlimb lameness by a rider actually are lame in front, but convincing a disbelieving trainer is difficult. Similarly, lameness perceived as “up high” (in the upper hindlimb, pelvis, or back) in most horses originates from the lower part of the hindlimb. The veterinarian must understand that everyone is trying to resolve the problem, but sometimes diplomacy is needed for successful communication. The veterinarian must be forthright and objective to determine the current source of lameness, even if the determination contradicts well-intentioned but strong-willed trainers. Clinical history is important but should not override clinical findings. In racehorses that perform at high speed, physical examination generally supports the finding that a horse bears away from the source of pain. During counterclockwise racing or training and with left forelimb lameness, a Thoroughbred (TB) will lug out (away from the inside of the track) and a Standardbred (STB) will be on the “left line” (bearing out; the driver must pull harder on the left line). Some horses, however, especially STBs with medial right forelimb pain, bear out particularly in the turns, presumably because the source of pain is medial or on the compression side of the limb. The veterinarian must seek out as much information as possible, particularly if the problem is complex or not readily apparent. Videotapes are useful, particularly if the gait deficit, behavioral problem, or any other circumstances necessary to elicit the suspected lameness cannot be duplicated during the examination. Paraprofessionals working with the horse provide useful information, but not everyone may agree about the source of the problem, and in some instances diplomacy is key to negotiating among concerned individuals.

CLINICAL HISTORY: BASIC INFORMATION Signalment Age

The age, sex, breed, and use of the horse are basic vital facts (Box 3-1). Flexural deformities, physitis, other manifestations of osteochondrosis, and angular limb deformities are age-related problems. Infectious arthritis (hematological origin), lateral luxation of the patella, and rupture of the common digital extensor tendon are conditions usually unique to foals. Emphasis on training skeletally immature, 2- and 3-year-old racehorses causes predictable soft tissue and bone changes, often resulting in stress-related cortical or subchondral bone injury. Liautard observed more than 100 years ago: “When an undeveloped colt, whose stamina is not yet established and constitution not yet confirmed, with tendons and ligaments relatively tender and weak, and bones scarcely out of the gristle, is unwisely condemned to hard labor, it is irrational to expect any other results than lesions of one or another portion of the abused apparatus of locomotion. They will be fortunate if they

Chapter 3  Anamnesis (History)

9

BOX 3-1 

Anamnesis: Basic and Specific Information Basic Information Signalment: age, sex, breed, use Current lameness: what is the problem? History of trauma Duration of lameness Deterioration or improvement of lameness Circumstances when lameness worsens or improves Effects of exercise: worsening or improvement in lameness Management changes Changes in shoeing and related issues Changes in training or performance intensity Changes in surface Changes in diet and health Changes in housing Current medication and response; response to rest Past lameness problems Specific Information Type of sporting activity Level of competition: current and future Additional sources Videotapes Images Records Discussions with others

BOX 3-2 

Summary of Lameness Conditions of the Geriatric Horse Chronic, progressive osteoarthritis Proximal and distal interphalangeal joints Metacarpophalangeal joint Carpometacarpal joint* Coxofemoral joint* Femorotibial joints Tarsus Progressive osteoarthritis—previous injury (usually retired racehorses) Navicular disease Unexplained, severe soft tissue injuries* Superficial digital flexor tendonitis Flexural deformity Suspensory desmitis Fractures during recovery from general anesthesia *Some of these conditions are unique to the older horse and often are unexplainable.

escape a fate still worse, and become sufferers from nothing worse than mere lameness.”1 This statement aptly summarizes the situation then and now. The high value of races for 2- and 3-year-olds results in high-intensity training for early 2-year-olds, which may result in injury such as maladaptive or nonadaptive remodeling of the third carpal bone (C3), precluding racing at a young age. Some problems are unique to older horses (Box 3-2). Overall, osteoarthritis (OA) and other degenerative

References on page 1255

10

PART I  Diagnosis of Lameness

Fig. 3-1  •  An aged Thoroughbred broodmare with severe forelimb deformity caused by primary severe osteoarthritis of the right metacarpophalangeal joint and secondary or compensatory (chronic overload) carpus varus in the left forelimb.

conditions such as navicular disease are most common but certainly are not unique to the geriatric horse. Some horses have a remarkably early onset of navicular disease or OA despite little physical work, suggesting a genetic predis­ position to the condition. These problems worsen with advancing age, particularly if several limbs are involved. In former racehorses, progressive OA is of particular concern; this condition most commonly affects the carpal and metacarpophalangeal joints (Figure 3-1). Occasionally in older horses, severe, progressive OA of the carpometacarpal joint occurs without any history of carpal lameness (Figure 3-2). In some horses, angular deformities (the most common is carpus varus) develop at the carpometacarpal joint. Inexplicably severe OA of the carpometacarpal and middle carpal joints is most commonly seen in Arabian horses (see Chapter 38). Primary OA of this joint is rare in young horses, even in racehorses with middle carpal joint abnormalities, unless C3 slab fracture or infectious arthritis occurs. OA of the coxofemoral joint is rare in horses with the exception of young horses with osteochondrosis, but it does occur in older horses. An unusual group of soft tissue injuries of unknown origin occurs in older horses. Superficial digital flexor tendonitis and suspensory desmitis generally are considered overuse injuries and usually occur in upper-level performance horses or racehorses. However, severe tendonitis and desmitis do occur, often suddenly and without provocation, in older (teenage) horses. Horses usually are turned out at pasture when initial lameness is observed. In some horses, superficial digital flexor tendonitis is severe and progressive, later leading to flexural deformity because of adhesions. Suspensory desmitis may be unilateral or

Fig. 3-2  •  Dorsopalmar digital radiographic image of the right carpus in a 13-year-old Arabian mare with pronounced lameness as a result of severe, progressive osteoarthritis of the carpometacarpal and middle carpal joints (medial is to the right). There is substantial varus limb deformity present. Comfort improved after partial carpal arthrodesis. (Courtesy Dr. Dean Richardson.)

bilateral, may involve the forelimbs or hindlimbs but is more common in the hindlimbs, and is most common in the older broodmares. The name degenerative suspensory (ligament) desmitis (DSD) was given to a syndrome, often seen in older horses and most common in Peruvian Pasos, in which severe, often bilateral suspensory desmitis occurred2-4 (see Chapter 72). In a recent study horses other than Peruvian Pasos were affected, and an alternative name—equine systemic proteoglycan accumulation—was proposed, because abnormal accumulation of proteoglycans in many connective tissues was found.4 However this has recently been disputed5; the suspensory ligaments (SLs) and other tissues from affected Peruvian Pasos and unaffected STB and Quarter Horses were examined using Safranin-O staining for detection of proteoglycan. Proteoglycan deposition was not unique to the affected Peruvian Pasos, being present in the nuchal ligament, heart, muscle, and other tissues, with similar or greater amounts in the control horses. However greater amounts were detected in the SLs of affected horses compared with control horses. It was concluded that cartilage metaplasia and associated proteoglycan deposition in affected SLs was the response to injury rather than the cause. Further work is needed to define this important disease. Older horses, particularly older broodmares, are at greater risk than younger horses to fracture long bones during recovery from general anesthesia.6 From 1988 to 1994, 9 of 14 horses with catastrophic fractures or dislocations that developed during recovery from general anesthesia were older than 10 years of age.

Age prominently affects prognosis. A common premise in considering lameness in foals is that young horses have time to outgrow the problem. Maturation will aid in angular limb deformities, some forms of osteochondrosis, and distal phalanx and diaphyseal fractures. However, fractures of important physes such as the proximal tibia may result in progressive angular deformities or disparity in limb length, limiting future prognosis. Early surgical management of flexural deformity of the distal interphalangeal (DIP) joint before 6 to 8 months of age optimizes future soundness and the possibilities for normal hoof conformation. In one study the reported success rate was 80%.7 If surgical management is undertaken later in life or when deformity is severe, the prognosis decreases substantially. The prognosis for survival of foals treated for infectious arthritis is reasonable, but only 31% of TB foals and 36% of STB foals started one or more races, indicating that the prognosis for future racing performance is poor, because articular healing even in young foals is not possible.8 In middle-aged (12 to 18 years of age), upper-level performance horses, prognosis is difficult to assess, particularly in horses with several problems. Level of competition rather than age may be the most important factor, and often performance level declines.

Sex

Most lameness conditions affect stallions, geldings, and mares with similar frequency. Sex-specific conditions are unusual but do exist. The most important consideration, however, regarding the horse’s sex is future breeding potential or lack thereof in the case of geldings. In many types of horses, and specifically in racehorses, decisions about future performance or racing potential often are important when management options and financial aspects are considered. This factor is particularly important when life-or-death decisions must be made after catastrophic injury (see Chapters 13 and 104). Frank discussions about the prognosis for return to the current sporting activity or level of performance often are necessary, and the clinician should consider reproductive capability of the horse. Owners are more likely to refrain from racing females and elect treatment for geldings and, in some instances, stallions. Future stallion prospects usually must prove race or performance success, thereby putting pressure on trainers to continue horses in training or racing. Behavioral abnormalities associated with the estrous cycle in fillies or mares are well recognized and may cause performance problems confused or misinterpreted as lameness (refusing fences, going off stride, striking) (see Chapter 12). An ill-defined behavioral problem in middle-aged nonracehorse mares could explain sudden performance problems often associated with or misinterpreted as lameness.9 Recurrent exertional rhabdomyolysis (RER) is more common in female TB racehorses10 and event horses.11 An association between sex and RER in STBs may exist and RER may be more common in fillies administered anabolic steroids. Obscure or unexplained hindlimb lameness has been attributed, rightly or wrongly, to retained testicles. The origin of lameness in these horses is difficult to prove without removing the retained testicle, and anecdotal reports suggest that hindlimb lameness has resolved after

Chapter 3  Anamnesis (History)

11

castration in some horses. The origin of pain in an abdominal cryptorchid is difficult to explain and questionable. The source of pain may be easier to understand in a horse with a testicle located within the inguinal canal. Activity of the external and internal abdominal oblique muscles and tension on the spermatic cord are possible explanations.

Breed and Use

Most lameness conditions affect all breeds of horses. Although breed has considerable influence on sporting activity, sporting activity or use primarily has the greatest impact on lameness distribution (see Chapters 106 through 129).

Current Lameness Determination of the Problem

Accurate information is necessary to determine precisely the horse’s current problem. Obtaining reliable information may be difficult if the horse has been purchased recently, if the horse has been claimed or changed trainers, or if you are giving a second opinion and have no past history with the horse. Additional objective information may be necessary to assess the effect of lameness on the horse’s performance. Evaluation of the horse’s race record may indicate when the problem began and if it is ongoing or new. The groom, rider (if not the owner), assistant trainer, blacksmith, and other paraprofessionals may have other pertinent information. Horses with poor performance usually are lame, although respiratory problems, rhabdomyolysis, shoeing, tack or equipment, and other medical problems can contribute. The horse’s past history is important in determining the cause of the current problem, particularly in racehorses training or racing with existing low-grade OA that develop new overload injury to supporting limbs (secondary or compensatory lameness). Existing problems such as OA worsen insidiously but may reach critical levels, causing sudden, severe unexpected lameness. OA of the metacarpophalangeal joint may exist for months in racehorses without causing obvious lameness, although in many horses joint effusion ultimately leads to treatment (“maintenance injections”). The horse suddenly may be much lamer after racing or training, and the trainer may assume the cause is different. Because intraarticular analgesia may only partially relieve lameness, persuading the trainer that the problem is still the fetlock may be difficult. Horses can endure extensive cartilage damage in any joint for many months, but at some point they reach a threshold level beyond which they cannot tolerate the pain.

History of Trauma

Many lameness problems develop during or shortly after a traumatic incident, but unfortunately many owners presume trauma played a role even when no one witnessed an alleged incident. A common but often erroneous assumption when examining a lame foal is that the dam stepped on it, but usually infection is the cause. Clinical signs of osteochondritis dissecans of the shoulder or stifle often are expressed after a traumatic incident, and yet most lame weanlings or yearlings are assumed to be lame because of trauma, not a developmental problem. Some lameness

12

PART I  Diagnosis of Lameness

problems appear after specific forms of trauma. Palmar carpal fractures occur most commonly in jumpers, but horses recovering from general anesthesia are at risk for this injury. Horses may be only mildly lame immediately after recovery, and the extent of injury is often not discovered until nonsteroidal antiinflammatory medication is discontinued, sometimes 7 to 10 days after the surgical procedure. A common history of horses with subluxation of the scapulohumeral joint (often called Sweeny or suprascapular nerve injury) is sudden profound lameness after being outside in a thunderstorm. Injury likely occurs when a horse runs into a solid object such as a tree, fence post, or building.

Duration

The veterinarian must understand the duration of the current lameness problem and determine whether a preexisting chronic, low-grade lameness exists and a sudden exacerbation of this problem has occurred, or a completely unrelated new problem has developed.

Worsening of Condition

The veterinarian must establish if the horse’s current problem is worsening or improving, under which con­ ditions or circumstances the lameness deteriorates or improves, and if the horse responds to treatment such as shoeing or management changes. Most lameness problems worsen with time, particularly if training or performance continues despite owner or trainer recognition. Racehorses with stress-related bone injury often are noticeably lame after work but become sound relatively quickly, within 1 to 3 days. A minimal number of other clinical signs are present, particularly because the most commonly affected bones (tibia, humerus) are difficult to palpate and buried by soft tissue. This cycle of lame-sound-work-lame is an important part of the history. Improvement of lameness with rest is important from historical and therapeutic perspectives. Lameness in most horses with severe articular damage, usually from severe OA, does not improve substantially with rest. Severe OA most commonly appears in the fetlock, femorotibial, and tarsocrural joints. Horses with fractures or mild to moderate soft tissue injuries generally improve with rest.

Warming into Lameness

Warming into lameness means the horse’s lameness worsens during the exercise period. Warming out of lameness means the lameness improves. This concept is important. Lameness associated with stress or incomplete fractures, soft tissue injuries (tendonitis and suspensory desmitis), splints, curb, and foot soreness worsens with exercise. In racehorses a worsening lameness appears as progressive bearing in or out during training or racing. In riding horses, this may be progressive stumbling, problems taking leads, progressive asymmetry in diagonals, or refusing to jump later fences. Horses with OA may be stiff and obviously lame at a walk, but lameness may improve with work. In western performance horses, OA of the proximal and distal interphalangeal joints and in some horses navicular syndrome cause lameness with this characteristic. The most dramatic example is distal hock joint pain, particularly in racehorses. Horses may be noticeably lame at a walk and trot, warm out of the lameness to the point of racing

successfully, and then show pronounced lameness after a race. One frequent statement at the racetrack is that the horse throws the lameness away at speed. This decrease occurs with some lameness conditions, such as distal hock joint pain, but two other factors are important. A horse may be able to race with lameness but not be able to perform at peak, particularly if lameness is bilateral. Horses often can race with bilateral conditions and show minimal signs of lameness, but performance is reduced. Lameness at the gallop may be impossible to perceive, and even at the fast trot or pace, most persons have difficulty seeing lameness. The same limitation occurs in observing a dressage or jumping horse at the canter. The veterinarian may gain some information by observing that a horse is reluctant to take either the left or right lead, but lameness is difficult if not impossible to detect at the canter. Unless slow-motion video analysis is available, the horse appears to be able to “throw lameness away,” but lameness is present but difficult to see. In this situation, horses do not warm out of lameness but simply cope with the pain while racing. Horses in this situation are at risk for developing compensatory problems. Older horses with OA may have difficulty in getting up and later may warm out of the lameness. Horses of any age with pelvic fractures or severe lameness may have difficulty in rising.

Recent Management Changes

Many lameness conditions start after a change in management. Changes in shoeing, training or performance intensity, surface, housing, and diet or other medical issues can have a profound effect on the musculoskeletal system. Changes in ownership often dictate changes in exercise intensity and certainly in owner expectations. The veterinarian must be careful in questioning and responding to questions if a horse has been purchased recently, especially if a colleague performed a prepurchase examination. Clinicians should avoid implying that a condition may have been preexisting or missed.

Shoeing The veterinarian should determine when the horse was last shod and whether the shoeing strategy was changed. Nail bind often causes acute progressive lameness related temporally to shoe application. Abscesses that result from a “close nail” may take several days to cause lameness. Foot balance is critical and, in some horses, changing foot angles results in lameness. A substantial increase or decrease in heel angle in a horse with chronic laminitis may exacerbate lameness. In horses with palmar foot pain, raising the heel angle may produce an obvious improvement in clinical signs briefly, whereas in horses with subchondral pain of the distal phalanx, raising the heel may worsen clinical signs. In racehorses with “sore feet” resulting from soft tissue and bone pain, changing shoes may result in improvement, related in part to temporary reduction in weight bearing in the painful area of the foot. Temporary lameness often occurs in horses with recently trimmed but unshod hooves, particularly if the horses’ hooves are trimmed aggressively or the ground is unusually hard for that time of year. The veterinarian must

Chapter 3  Anamnesis (History)

remember that a horse with recently trimmed hooves often shows bilateral forelimb lameness when trotted on flat or uneven hard surfaces, regardless of the primary cause of the current lameness. The horse should be reassessed on a soft surface. Attempts to make both front feet symmetrical may create substantial lameness immediately after trimming. Horses may cope well with different size and shaped front feet, but when radical trimming is performed, they may develop severe lameness. The veterinarian must determine whether any recent or past changes in shoeing either improved or worsened lameness. Lameness in a STB trotter with foot pain may be improved by changing from conventional shoes, such as half-round or flat steel shoes in the front to a “flip-flop” shoe. The farrier often first notices a common problem that a horse is reluctant to pick up the hindlimbs. In some horses this problem is purely behavioral, whereas in others it is a real sign of pain. This history most often is associated with conditions such as OA of one or more joints but also may be a sign of pelvic or sacroiliac pain. In Warmbloods, draft breeds, and draft-cross horses, reluctance to pick up a hindlimb may be an early sign of shivers.

Training or Performance Intensity Lameness that worsens in response to recent increase in training intensity may be related to stress-related subchondral or cortical bone injury. Stress fractures, bucked shins, or maladaptive or nonadaptive stress-related injuries of subchondral bone occur typically during defined periods of training and often after brief periods of rest. When horses in active race training are given time off, even brief periods such as 7 to 21 days, bone undergoes detraining, leaving it subject to stress-related injury. If training resumes at the prerest level or is accelerated, stress fractures or bucked shins often develop. In 3-year-old TBs, stress fractures of the humerus often occur within 4 to 8 weeks after returning to training. Bucked shins often develop in 2-yearold TB racehorses after a brief rest period for an unrelated medical condition.

Surface Most lameness conditions worsen if the horse performs on a harder surface. In show horses such as the Arabian or half-Arabian breeds, foot lameness often results when horses are warmed up or shown on harder surfaces. An association exists between fracture development and hard racing surfaces. A dramatic change in any racing surface may lead to unexpected episodic lameness in racehorses. On breeding farms, anecdotal evidence suggests drought conditions causing harder than normal pastures lead to a higher prevalence of osteochondrosis or distal phalanx fractures. Lameness that is most pronounced on hard surfaces is often seen with conditions of the foot. Lameness that worsens on softer surfaces, however, may be associated with soft tissue injuries such as proximal suspensory desmitis. Uneven surfaces may exacerbate lameness and other gait abnormalities. Horses prone to stumbling on uneven surfaces may have palmar foot pain, proximal suspensory desmitis, or neurological disease. Horses with bilateral lameness may be lame in one leg going in a particular

13

direction on a banked surface (such as a racetrack) and lame in the opposite leg going the other way. Bilateral lameness may be confused with other causes of poor performance because of inconsistencies in gait. Lameness may worsen or improve when a horse goes uphill or downhill.

Diet and Health Changes in diet or dietary factors may lead to or exacerbate existing lameness conditions. Dietary factors, especially dietary excesses or deficiencies, are important in the many manifestations of developmental orthopedic disease (see Chapter 55). Sudden changes in diet, such as those associated with turning horses out on lush pastures or consumption of large quantities of grain (grain overload), may cause laminitis or exacerbate existing chronic laminitis. Overweight horses normally consuming a high-grain diet may be prone to laminitis or gastrointestinal tract disturbances that lead to laminitis. Lameness may be associated with, or result from, other medical conditions. Obvious associations exist in foals; for example, conditions such as infectious arthritis and physitis are associated with umbilical, gastrointestinal, or respiratory tract infections. Immune-mediated synovitis also occurs in older foals with chronic infections (see Chapter 66). In adult horses, infectious arthritis generally develops after intraarticular injections or penetrating wounds, but may result from hematological spread of bacteria. Occasionally, horses develop distal extremity edema and lameness after vaccination, presumably caused by vasculitis or other immune-related mechanisms. Similar signs appear in horses with purpura hemorrhagica or viral illnesses such as equine viral arteritis.

Housing Many lameness conditions develop while a horse is turned out, or as the result of turnout, often as the result of trauma such as kick wounds or fence-related injuries. Sudden changes in weather may excite horses, particularly those turned out at pasture. Minimizing problems with turnout requires the use of well-groomed and well-maintained pastures or paddocks with individual paddocks to reduce horse-to-horse interactions. Dramatic housing changes have a substantial impact on the development of lameness. Shipping to and from sales, foaling, and weaning are associated with soft tissue injuries, puncture or kick wounds, and other injuries.

Current Medication Changes and Response

The veterinarian must establish if the horse currently is receiving medication or was administered medication recently and the response to treatment. Response to medication or a management change is important information in formulating a treatment plan. For example, recent improvement with rest and the administration of nonsteroidal antiinflammatory drugs indicates more of the same treatment may be reasonable. The veterinarian must establish dosages of medication because a horse may not respond to phenylbutazone because of underdosage. Many owners and trainers do not understand that although intraarticular analgesia relieves lameness, intraarticular medication may not, thus causing doubt about the diagnosis. This characteristic commonly appears in horses

14

PART I  Diagnosis of Lameness

with subchondral bone pain and is useful in diagnosis. Horses with early OA and negative or equivocal radiological signs, or those with short, incomplete fractures, often do not respond to intraarticular medication. Negative radiological findings are a good sign because dramatic radiological evidence of subchondral lucency or fracture reduces the prognosis considerably. However, convincing the trainer of the validity of the diagnosis may be difficult. The amount of rest is important. Many acquired conditions, such as OA, or degenerative conditions, such as navicular syndrome, take many months and usually years to develop. Therefore expectation that a horse will show marked improvement with a brief rest period is unreasonable. Lameness in many horses with severe OA may not improve substantially, even with prolonged rest. In horses with early OA in which pain occurs primarily in subchondral bone and for which radiological findings are negative or equivocal, rest or controlled exercise for 3 to 6 months may be necessary. The same regimen applies for horses with navicular syndrome, fractures, and many soft tissue injuries. Quality of rest is equally important. Did the horse receive absolute box stall rest with handwalking, or was it

A

lunged or turned out in a paddock or field with other horses? Was a brief rest period followed by an attempt to ride or train the horse? Those associated with the horse often consider this type of intermittent rest complete rest, but many conditions remain chronically active. Without adequate rest, reinjury follows temporary improvement and early healing, highlighting that, in my opinion, turnout is the antithesis of healing!

Past Lameness History

Obtaining the horse’s entire lameness history may not be necessary or possible, but the veterinarian should gather as much information as is practically available. Prognosis for many injuries is affected adversely by recurrence, and often management options differ in these situations. Recurrence may prompt more aggressive therapy, considerations for referral, or perhaps surgical evaluation if the problem involves a joint. If a reliable diagnosis was made previously, retreatment for the past problem may be a reasonable or preferred management approach, particularly between races or competitions. If a horse responded previously to intraarticular medication, reinjection may be reasonable. However, in many horses with progressive OA, results of

B

Fig. 3-3  •  Initial (A) and 2-week follow-up (B) dorsopalmar radiographic image of the left third metacarpal bone in an 18-year-old Thoroughbred gelding. The initial image was obtained after the horse was found to have a small skin wound in the region but was sound. Acute, severe lameness developed 9 days after initial injury, and the follow-up radiograph shows a long oblique fracture of the third metacarpal bone. (Courtesy Dr. Janet Durso, 2001.)

Fig. 3-4  •  Craniocaudal radiographic image of the left antebrachium of a 5-year-old Thoroughbred mare showing a displaced, long oblique  fracture of the radius. This filly had sustained a small puncture wound to  the lateral aspect of the antebrachium 5 days earlier but was sound. The mare was turned out and developed acute, severe lameness and was later euthanized.



Chapter 4  Conformation and Lameness

additional therapy often are diminished. The veterinarian should not assume that the failed response to intraarticular medication means the problem lies elsewhere because medication does not affect subchondral bone pain in early or late OA. Recent history is important. Small, innocuous-looking wounds over the third metacarpal bone or third metatarsal bone, radius, or tibia may be associated with bone trauma with delayed-onset severe lameness. Incomplete or spiral fractures may develop from small cortical defects (Figure 3-3). Catastrophic failure of long bones occurs even when initial radiographs show no or minimal cortical trauma. The radius appears to be at greatest risk (Figure 3-4).

15

New problems may and often do arise despite a long history of recurrent lameness. Comprehensive reevaluation is the best and safest approach to avoid delays in proper diagnosis and treatment.

FURTHER INFORMATION Full understanding of a horse’s use, type and level of sporting activity, and value, all of which help the veterinarian assess prognosis, requires specific information. If a horse previously was under the veterinary care of another individual in the same or a different practice, it is important to obtain accurate case records and view previous radiographs and other images.

Chapter

4 

Conformation and Lameness Mike W. Ross and C. Wayne McIlwraith

References on page 1255

The idea of a good horse with poor legs is a misnomer; the legs are the essence of the horse, and every other part of the equine machine is of only subservient and tributary importance. A. Liautard1

The thought that the way a horse is conformed determines the way it moves is well accepted. The relationship of conformation, especially of the distal extremities, and lameness also is well recognized. “Conformation determines the shape, wear, flight of the foot, and distribution of weight.”2 Veterinarians often are asked to comment on conformation during lameness and prepurchase examinations, especially with regard to the suitability of the horse to perform the intended task. In some instances, as in the case of presale yearling evaluations, the veterinarian’s opinion is paramount, and purchase is contingent on judgment of the yearling’s potential to perform as a racehorse, given its conformation, or in some instances its conformational faults (see Chapter 99). “It is by a study of conformation that we assign to a horse the particular place and purpose to which he is best adapted as a living machine and estimate his capacity for work, and the highest success in this connection will be best attained by the judicious blending of practice with science.”3 Evaluation of conformation and its influence on lameness is based largely on observation, experience, and pattern recognition. Recognizing desirable conformational traits in horses suited for a particular sporting activity and learning when to overlook a minor fault that has little clinical relevance are important.

RELEVANCE OF EVALUATION OF CONFORMATION Conformation is one piece of the complex puzzle of a lame horse, although poor conformation does not necessarily condemn a horse to lameness: “faulty conformation is not an unsoundness … it is a warning sign.”2 All lameness diagnosticians should evaluate conformation briefly at the beginning of each examination. The association of lameness and faulty conformation will be obvious. The clinician must evaluate the horse from afar, assessing the whole horse for balance, angles and lengths, and posture and symmetry. The clinician must remember that horses come in all shapes, sizes, and types, and therefore conformation varies accordingly, but certain conformational faults produce predictable lameness conditions and are undesirable. However, good conformation is not synonymous with success, and although horses of certain body types tend to have longer strides and are more athletic than others, intelligence, aggression, “will to win,” and other intangible factors are important. It is our opinion that a well-bred horse from a successful family can endure faulty conformation much better than one with poor or mediocre breeding.

HEREDITARY ASPECTS OF CONFORMATION Certain conformational faults appear to be highly heritable traits. Evaluation of broodmares and foals often reveals that the early conformational defects seen in a foal are present in the dam. The dam seems to contribute more to faulty conformation than does the sire, although the stallion also is important. This difference may be explained in part by the fact that fillies with faulty conformation may develop problems or be retired early and subsequently bred, whereas most stallions usually are proven performers with exceptional conformation. Conformational faults such as toed in and toed out commonly are passed down from generation to generation. Back-at-the-knee (calfknee), offset (bench) knee, tied-in below the knee, sicklehocked, and straight-behind conditions appear to be highly heritable. In a recent study abnormal sire phenotype (offset carpi and outward rotation) was associated with faulty

16

PART I  Diagnosis of Lameness

yearling carpal conformation.4 Heavier foals and yearlings were more likely to have faulty carpal conformation and inward rotation of the fetlock joints.4 Certain lameness conditions are common in horses with faulty conformation, but similar lameness conditions develop inexplicably in some breeding lines year after year in offspring with apparently acceptable conformation. Lameness of the carpus or tarsus appears to be most important. For example, in Standardbreds (STBs), siblings commonly develop similar lameness conditions, such as proximal suspensory avulsion injury, carpal osteochondral fragments, distal hock joint pain, or curb.

OBJECTIVE EVALUATION OF CONFORMATION: IS IT POSSIBLE? An attempt to quantify conformation using a linear assessment trait evaluation system that allows the observer to assess where, given a particular trait, a single horse falls within a population of horses, was described in 1996.5 A population of 101 Irish Thoroughbred (TB) flat racehorses and 19 top stallions was used and 27 common conformational traits were evaluated, including various heights, lengths and angles, and distal extremity conformation. Of the 27 traits, six were significantly linked to age (withers’ height and conformation, back length, neck size, carpal conformation, and hind pastern conformation), and five were linked to sex (head and neck shape; neck size at the poll, the larynx the withers, and the manubrium of the sternum; and forelimb hoof pastern axis). Most traits exhibited large phenotypic variation within the population, but 21 of 27 non–age-linked traits were judged suitable for possible inclusion in a linear assessment protocol.4 Researchers judged a high percentage of horses to be toed out, suggesting this trait may even be desirable. More recent studies have used video-image analysis, but direct physical measurements may be more accurate than those obtained by analyzing videotapes or photographs.6 Potential errors in image analysis occur because of movement of skin markers over selected bony protuberances, a phenomenon more common in the upper limb and in motion studies.6,7 Skin marker location is critical for evaluation of joint angulation and movement during locomotion or conformation analysis. Instantaneous center (or axis) of rotation (ICR) is defined as the point with zero velocity during movement of that joint; accurate measurements of joint angulation require positioning markers at the ICR.8 Conventional positions of skin markers and ICR in most joints agree well, but use of traditional marker sites on the scapulohumeral and femorotibial joints results in overestimation and underestimation, respectively, of caudal joint angles.9 Although video-image analysis may be fraught with potential or in some instances real error, objectivity is a major advantage. Other advantages include the ability to replay images, reduction of observer fatigue, elimination of observations and measurements in real time, and permanent recording of the observation. Ideally, objective measurements would withstand statistical evaluation, distinguish between desirable and undesirable traits, and account for differences among different types of horses.6 A combination of direct measurement and photo­ graphy was used to evaluate conformation of Swedish

Warmblood (WBL) and elite sports horses.10,11 Whereas most of the conformational defects were mild or moderate, 80% of WBL horses were toed out behind, suggesting this may be a normal finding in this breed as in the STB trotter. More than 50% of horses had bench knees and 5% were toed out in front, contrary to findings in STB trotters.10,12 Many of the elite horses were bucked kneed, whereas the riding school horses tended to have calf-knees. It was speculated that this occurred because elite horses were evaluated after competition, and muscle fatigue may have contributed to the tendency to be over at the knee. Sex had a significant influence on conformation; females were smaller and had longer bodies and smaller forearms and metacarpal regions. There were interesting findings regarding hock angle. A sickle hock is defined as a hock angle of 53 degrees or less; a large hock angle is referred to as straight behind. Sickle-hocked conformation was nearly absent in elite horses, and it was hypothesized that sickle-hocked conformation either predisposed a horse to lameness or impaired a horse’s ability to achieve upper levels of competition.10 A positive relationship between larger hock angles and soundness in STB trotters also exists.13 All results must be viewed in moderation, because it is our clinical impression that horses with excessively large hock angles (straight behind) are substantially predisposed to suspensory desmitis. In forelimbs of WBL show jumpers and the forelimbs and hindlimbs of STB trotters, smaller fetlock joint angles (less upright) were desirable.10,13 Radiology was used to assess the degree of hyperex­ tension of the carpus to study the potential effect of backat-the-knee (calf-knee) conformation on the subsequent development of carpal chip fractures.14 Lateromedial radiographic images of 21 horses with carpal chip fractures and of 10 normal horses were obtained, with and without the contralateral limb raised. No relationship between measured carpal angle and carpal chip fracture formation existed, suggesting that this group of TB racehorses did not develop carpal chip fractures as a result of calf-kneed conformation. The sample size was small, however, and a larger study may produce different results. Horses with severe calf-kneed conformation may develop other problems and not advance enough in training to develop carpal chip fractures. They may be judged poor surgical candidates, are not referred, or are slow. Two recent studies evaluated TBs and Quarter Horses (QHs) using skin markers, photography (three views: front, side, back), and computer-image analysis.15,16 Of the two studies done in TBs, one evaluated longitudinal development of conformation from weaning to 3 years of age. A strong relationship between long bone lengths and withers heights for all ages supported the theory that horses are proportional. Longitudinal bone growth in the distal limb increased only 5% to 7% and was presumably completed before the yearling year. Withers height, croup height, and length of neck topline, neck bottom line, scapula, humerus, radius, and femur increased significantly from age 0 to 1 year and age 1 to 2 years. Hoof lengths (medial and lateral, right and left) grew significantly from the ages of 0 to 1 and 1 to 2 years but decreased in length from age 2 to 3 years (presumably associated with trimming).15 Changes in growth measures indicated that growth rate either slowed or reached a plateau at 2 to 3 years of age. Horses also became more offset in the right forelimb between weaning



Chapter 4  Conformation and Lameness

and age 3, but the offset ratios did not change with age in the left forelimb. Shoulder angle increased in all age groups (becoming more upright), and this contributed to the increase in measured height at the withers. Dorsal hoof angle (both front and hind) decreased significantly from ages 0 to 1 and 1 to 2 years but did not change in the 2and 3-year-old groups. This study provided objective information regarding conformation and skeletal growth in the TB, which could potentially be used for selection and recognition of important conformational abnormalities.15 Measurements of length and angle were obtained from photographs in which a tape measure was used for objective criteria and an objective method was developed for measuring offset knees (Figures 4-1 to 4-4).15 In another study the role of conformation in the development of musculoskeletal problems in the racing TB was evaluated.16 Conformation measurements were obtained

17

from photographs of horses with markers at specific reference points and digitally analyzed as previously described.15 Clinical observations were recorded regularly for each horse, and stepwise (forward) logistic regression analysis was performed to investigate the relationship between binary response of clinical outcomes probability and conformation variables by the method of maximum likelihood. Clinical outcomes significantly (P < .05) associated with conformational variables included effusion of the front fetlock joints, effusion of the right carpal joint, effusion of the carpal joints, effusion of the hind fetlock joints, fractures of the left or right carpus, and right front fetlock and left hind fetlock lameness. Offset knees contributed to fetlock lameness (for every 10% increase in the right offset ratio, the risk of effusion in the right front fetlock increased 1.8 times and the odds of right front fetlock lameness increased by a factor of 1.26). Long pasterns increased the odds of forelimb fracture. Surprisingly, an increase in the carpal angle as viewed from the front (carpus valgus) appeared to act as a protective mechanism, because odds for the development of carpal fracture and carpal effusion decreased with increase in carpal angle (for every 1 degree increase in right carpal angle as viewed from the front, the odds of effusion in the right carpus decreased by a factor of 0.68 and the odds of a right carpal fracture decreased by a factor of 0.24).16 Horses with long shoulders had decreased odds of developing forelimb fracture (odds ratio [OR] = 0.50), but horses with long pasterns had increased odds for forelimb fracture (OR = 4.55). Long sloping pasterns were suggested as a potential cause of carpal chip fractures.14 In the second TB study described previously, ORs were created for increase in bone length of 2.54 cm (1 inch) or

Fig. 4-1  •  Length measurements (centimeters) recorded from the left lateral view in a Thoroughbred conformational study.15 (Reproduced with permission from Anderson TM, McIlwraith CW: Longitudinal development of equine conformation from weanling to age 3 years in the Thoroughbred, Equine Vet J 36:563, 2004.)

Fig. 4-2  •  Angle measurements (degrees) recorded from the left lateral view in a Thoroughbred study.15 (Reproduced with permission from Anderson TM, McIlwraith CW: Longitudinal development of equine conformation from weanling to age 3 years in the Thoroughbred, Equine Vet J 36:563, 2004.)

Fig. 4-3  •  Length (centimeters) and angle measurements (degrees) recorded from the front view in a Thoroughbred study.15 (Reproduced with permission from Anderson TM, McIlwraith CW: Longitudinal development of equine conformation from weanling to age 3 years in the Thoroughbred, Equine Vet J 36:563, 2004.)

18

PART I  Diagnosis of Lameness

Fig. 4-4  •  Lines drawn to determine offset ratios. A bench-knee measurement, called an offset ratio, of the medial width/lateral width determines the amount of third metacarpal bone that is offset laterally. The medial/ lateral width is the distance (centimeters) from a line drawn along the medial or lateral aspect of the third metacarpal bone to a line from the medial or lateral distal lateral radial physis parallel with the third metacarpal bone. A ratio of greater than 1.0 represents bench-kneed conformation. (Reproduced with permission from Anderson TM, McIlwraith CW: Longitudinal development of equine conformation from weanling to age 3 years in the Thoroughbred, Equine Vet J 36:563, 2004.)

joint angle of 1 degree and development of lameness.16 For every 2.5 cm increase in humeral length, odds for fracture of the proximal phalanx or carpal synovitis or capsulitis increased. Increased length from elbow to ground and increased toe length increased chances for carpal fracture, and in horses with offset knees greater than 10% the potential for carpal or fetlock synovitis or capsulitis increased. The potential for fracture of the proximal phalanx increased with an increase in shoulder angle.16 A study examining conformation in 160 racing QHs in training at Los Alamitos Race Course found humeral length had a significant association with several clinical entities.17 For every 10-cm increase in humeral length the odds of an osteochondral fracture fragment of the dorsoproximal aspect of the left front proximal phalanx increased by a factor of 9.06. Similarly, ORs for carpal synovitis and capsulitis and for sustaining carpal chip fracture (8.12 in the left forelimb and 10.17 in the right forelimb) rose significantly with each 10-cm incremental increase in humeral length. The length of the left front toe was important.17 For each 1-cm increase in toe length, the odds of sustaining carpal chip fractures increased by a factor of 58.90.17 Horses with upright shoulders were at increased risk for development of osteochondral fragmentation of the

proximal phalanx and those with offset carpi were at increased risk for development of synovitis and capsulitis in both forelimbs (OR = 2.26).17 The relationship of many lower limb lameness conditions with limb length is interesting and somewhat unexpected because longer limb length generally is considered desirable. In addition, a relationship between longer toes and carpal fracture is interesting. Longer toes may delay breakover of the foot, altering forelimb biomechanics, but an effect on a distant joint such as the carpus cannot be easily explained. The relationship between offset knees and lower limb lameness was expected, but unexpected were fewer carpal fractures in TBs with this conformational fault. Because development of lameness, termed clinical outcomes in these studies, is complex, confounding variables such as track conditions, training regimen, breeding, individual horse ability, and experimental error could have contributed to outcome. Little doubt exists that acquiring objective information is useful, not only to determine what is abnormal but also to define what is normal in a population. In both WBLs and STB trotters in Europe, toed-out conformation in the hindlimbs should likely be considered normal because a majority of both breeds have this conformational trait.10,12 These populations differed, however, in forelimb conformation. Few STB trotters had bench-kneed conformation, a finding supported by one of our (MWR) clinical observations that this conformational fault is highly undesirable in this breed (see Chapter 108). Recently, variation in conformation of National Hunt racehorses established guidelines with which individual horses could be compared and highlighted significant variations in horses with different origins (Irish and French horses differed significantly in girth and intermandibular width measurements).18 Circumference and length measurements were significantly associated with withers height. No underlying pattern of combinations of conformational parameters was found, but variations were identified between left and right measurements and in hoof, stifle angle, and coxofemoral angle measurements.18

EVALUATION OF CONFORMATION Conformation determines the way a horse moves, and it is intuitive that a relationship exists between faulty con­ formation and the development of lameness. Therefore assessment of conformation should be an integral part of lameness examination. Conformation evaluation has four basic components: assessment of (1) balance, (2) lengths, angles, and heights, (3) muscling, and (4) conformation of the limbs. All are intertwined but should be evaluated separately, considering the whole horse not just the limbs, and then consolidated. The clinician should evaluate the horse on firm, level ground, preferably a smooth, nonslip surface that does not obscure the view of the feet. The horse should stand squarely with equal weight on all four limbs. Dynamic assessment of limb conformation while the horse is walking also is essential.

Balance

Balance is the way all parts of the horse fit together and is linked directly with assessment of lengths, angles, and heights. The horse should be proportional and thus well

Chapter 4  Conformation and Lameness



19

X

Y

Z

Fig. 4-5  •  Diagrammatic depiction of assessing balance during conformation evaluation. Three circles (from left to right: forehand, midbody, hindquarters) are visualized and should overlap by approximately one third. Excessive overlapping of circles (short coupled) or scant overlapping of circles (long, weak in the back) are common conformational abnormalities. Body length (X) should be equal to or slightly longer than withers height (Y), and withers height and rump height (Z) should be the same.

balanced. A horse may be visualized in thirds—the forehand, the midbody, and the hindquarters—by drawing three circles incorporating these areas (Figure 4-5). The circles should overlap but not excessively. Horses in good balance are likely to be superior athletes. Horses with a short, thick (throatlatch and shoulder regions) neck are often heavy and straight in the shoulders (Figure 4-6). A horse with a short back has naturally closer dorsal spinous processes which may be predisposed to impingement or overriding, whereas a horse with a long back (Figure 4-7) may have difficulty engaging the hindlimbs properly. The clinician must assess the relative heights of the withers and hindquarters. A horse that is taller behind than in front (rump height is greater than height at the withers) is pre­ disposed to forelimb lameness. A horse that also is underdeveloped in the shoulders and upper forelimbs (weak up front) and heavy behind is more at risk. Limb lengths should be proportional to body size and height. In general, the body length (point of shoulder to point of rump) should be equal or slightly longer than withers height (see Figure 4-5). Head conformation is not relevant to lameness, but the size of the head relative to the body and the angulation between the head and neck influence the ease with which the horse can work “on the bit” (see Chapters 97 and 116). A horse’s ability to see is important. A horse with ocular abnormalities may exhibit bizarre behavioral abnormalities or unusual head and neck carriages, possibly misinterpreted as the result of pain. A rare cause of “being on a line” occurs in driving horses, such as a STB with unilateral

Fig. 4-6  •  Horse with short, heavy neck; heavy, short, and straight shoulder; and withers set forward. This horse is prone to forelimb lameness and likely to have a short stride.

blindness. The horse turns the head toward the blind side to see with the opposite eye and thus is on the contralateral line (to straighten the head, the driver must pull on the contralateral line). This mimics a contralateral (to the blind eye) lameness.

20

PART I  Diagnosis of Lameness

Lengths, Angles, and Heights

withers laid too far caudally. Horses should have adequate depth in the girth region (depth of girth). Shoulder length (top of the withers to the point of the shoulder) may be related directly to stride length, and horses with longer shoulders usually have longer strides (Figure 4-8). Those with short shoulders usually have shorter strides (see Figure 4-8). Shoulder length and shoulder angle often are related; long shoulders often are more sloping (smaller shoulder angle), and short shoulders often are straight. Good shoulder length appears to be important and desirable, but recent objective data from TB and QH racehorses suggest that horses with long limbs may be at increased risk for lower limb lameness.16,17 In TBs particularly a long radius (forearm) and short, strong third metacarpal bone (McIII) have been considered desirable for adequate strength and maximum stride length. However, more recent work16 suggests that a long forearm would lead to a long metacarpal bone, and because horses are proportional we must question this long-held impression. Chest width should be commensurate with overall body size. A wide chest with a base-narrow forelimb stance (the front feet are close when the horse is evaluated from the front) or a narrow chest with a base-wide stance are undesirable. In STB pacers a good chest width is desirable, but in trotters a narrow chest is preferred (see Chapter 108). Rump length also is important in determining stride length, and a longer length of the rump is desirable. Many horses with long rumps have larger rump angles (flat croup), and those with short rumps have smaller rump angles (steep croup). Long, flat croup regions are desirable. The ideal

Body length is important in determining stride length (see Figure 4-5). Short-coupled conformation predisposes horses to short strides and problems with interference, especially racehorses. If horses are too long, they can be weak in the back. The length of the neck is important in assessing balance and should be proportional to the overall body length. Some horses have long, weak necks. The neck may be “set on low” relative to the shoulder, with a depression (ventral deviation) of the dorsal topline cranial to the withers (ewe necked), giving the appearance of prominent

Fig. 4-7  •  Unbalanced Appaloosa gelding that is long and weak in the barrel (back). Rump height is slightly higher than withers height.

A

Rump length

Shoulder length

B

D Shoulder angle

Rump angle

C

Pastern angle

Stride length

E

Fig. 4-8  •  Measurement of shoulder length (A), rump length (B), shoulder angle (C), and rump angle (D). The pastern angle (E) should be equal to the shoulder angle. Shoulder angle and length are important in determining stride length.



Chapter 4  Conformation and Lameness

horse should have a long gaskin (crus) and a short, strong metatarsal region (the hocks close to the ground) to maximize stride length. The angles of the shoulder and rump are important factors in determining stride length and balance. Undesirable shoulder and rump angles often accompany other conformational faults and may predispose to lameness. The ideal angle of the shoulder (relative to the ground) has classically been determined to be 45 degrees (see Figure 4-8). Horses with steep shoulder angles (>50 to 55 degrees) usually have short shoulders and short, upright pasterns, which predispose to lower limb lameness. The forelimb pastern angle should be equal to the shoulder angle. A steep shoulder angle shifts the center of gravity forward, predisposing to forelimb lameness. Horses with a flat rump or croup generally have longer rump lengths and longer strides (Figure 4-9). Horses with short, steep rumps (goose rump) often have short, choppy gaits, and many have hindlimb lameness (Figure 4-10). A steep rump angle shifts the center of gravity caudally, predisposing to hindlimb lameness.

Limbs

It is critical to evaluate limb conformation with the horse standing squarely on a firm, flat surface and with an experienced handler who can make the horse cooperate. If the clinician observes a fault that may result from how the horse is standing, he or she should reevaluate the horse after repositioning. Horses often stand camped out, both behind and in front, simply as the result of improper positioning. The plumb line concept allows evaluation of each limb from the front or back and the side (Figure 4-11). For example, a vertical line from the point of the shoulder should bisect the limb. The clinician also should evaluate the horse while it is walking because some defects are dynamic. Horses that toe in or toe out, or those with fetlock or carpus varus deformities, may stand reasonably well, particularly with corrective trimming and shoeing,

Fig. 4-9  •  Desirable hindlimb conformation. The flat rump angle and good rump length would likely increase stride length and allow good support and strength of the hindlimbs.

21

but the defect may be readily apparent while the horse is walking.

FORELIMB CONFORMATION Front Perspective

Several forelimb conformational abnormalities are apparent when a horse is evaluated from the front. Base-wide conformation may occur alone or in combination with toed-in or toed-out conditions (Figure 4-12). Horses that are base wide stand with the forelimbs lateral to the plumb line and generally are narrow in the chest, resulting in overload of the medial aspect of the lower limb, predisposing to lameness. Horses that are base wide, toed in tend to wing out or paddle during protraction (Figures 4-12, B and 4-13, A). Winging out predisposes trotters to interference with the ipsilateral hindlimb. Base-wide, toed-out conformation appears most often in horses with uncorrected carpus valgus deformities (Figures 4-12, C and 4-13, B) and results in excessive loading on the medial aspect of the foot and misshapen feet. Interference with the contralateral forelimb may occur in severely affected horses. Base-narrow conformation may occur alone or in combination with toed-in or toed-out conformation (Figure 4-14). Horses that are base narrow stand with the forelimbs inside each plumb line and overload the outside of the lower limb and foot. Horses that are base narrow, toed in tend to wing out, and those that are base narrow, toed out tend to wing in during protraction (see Figures 4-13 and 4-14). With in-at-the-knee, knock-kneed, or carpus valgus conformation (Figure 4-15) the carpi are medial to the plumb

Fig. 4-10  •  Undesirable hindlimb conformation characterized by a short, steep rump (goose rump), predisposing to hindlimb lameness.

22

PART I  Diagnosis of Lameness

A

B

C

D

Fig. 4-11  •  Diagram demonstrating use of plumb lines to evaluate limb conformation from three perspectives. Vertical lines are visualized from A, the front forelimb (line runs from point of the shoulder, bisecting the limb), B, the side forelimb (line bisects elbow joint, carpus, and fetlock joint and intersects the ground approximately 5 cm behind the solar surface of the heel), and C, the side hindlimb (line runs from point of rump to the ground, touching the point of the hock and plantar aspect of the metatarsal region and intersecting the ground approximately 7.5 to 10 cm behind the heel) and from D, the back hindlimb (line drawn from point of rump, bisecting the hindlimb).

A

B

C

Fig. 4-12  •  Three variations of base-wide forelimb conformation, including (A) simple base wide, (B) base wide, toed in, and (C) base wide, toed out.

line, creating an angular deformity and concentrating the weight of the horse on the medial aspect of the carpus and proximal metacarpal region. This condition, if severe, may predispose the horse to carpal lameness and splints. However, recent objective data have suggested that a certain degree of carpal valgus is protective for synovitis and capsulitis, as well as chip fractures in the carpus.16 Predisposition to carpal lameness and splints with carpal valgus conformation probably applies only to horses with severe abnormalities. In some horses, particularly foals, carpus valgus may be accompanied by external rotation of the entire limb or just the distal aspect (toed out). Severely

affected horses wear the inside aspect of the hoof or shoe abnormally. Out-at-the-knee (bowlegged, bandy-legged) conformation usually is a consequence of early carpus varus and usually is career-limiting (Figure 4-16). The carpus is bowed outward, lateral to the plumb line. Many horses are also toed in, accentuating abnormal forces on the lateral aspect of the entire distal forelimb, predisposing to osteoarthritis (OA) of the carpus or fetlock or lateral suspensory branch desmitis and sesamoiditis. In most foals with carpus varus, there is coexistent lateral deviation of the elbow, giving the appearance that the angular deformity might be arising

Chapter 4  Conformation and Lameness



RF

RF

LF

23

LF

MIDLINE MIDLINE

A

B

Fig. 4-13  •  A, Toed-in conformation often causes horses to wing out or paddle during advancement of the forelimb. B, Toed-out conformation causes horses to wing in, predisposing to interference with the contralateral forelimb.

A

B

C

Fig. 4-14  •  Three variations of base-narrow forelimb conformation including (A) simple base narrow, (B) base narrow, toed in, and (C) base narrow, toed out.

from asymmetrical growth in the physes associated with the elbow joint. Correction is difficult but usually involves transphyseal retardation of the distal lateral radial physis. Offset or bench-knee conformation is classically defined as lateral positioning of the metacarpal region relative to the central axis of the radius (Figure 4-17). However, radiographs demonstrate that the actual displacement usually is at the antebrachiocarpal joint. Displacement may be

unilateral or bilateral with differing degrees of severity on each side. This conformation has been often associated with carpal or metacarpal lameness (Figure 4-18). Many 2-year-old STBs with offset knees are precocious during early training but often develop carpal lameness at 3 or 4 years of age. TBs with offset knees are believed to perform better on the soft turf tracks in Europe, as opposed to the firm turf or dirt tracks in the United States. In recent

24

PART I  Diagnosis of Lameness

Fig. 4-15  •  A horse with in-at-the-knee conformation that is worse in the right forelimb. Fig. 4-17  •  Standardbred with a prominently offset (bench) knee in the left forelimb. An apparent lateral deviation or shifting (offset) of the cannon bone and distal extremity occurs relative to the plumb line dropped through the left radius.

Fig. 4-16  •  Two-year-old Thoroughbred filly with moderate-to-severe carpus varus (out-at-the-knee) conformation in the left forelimb and mild deformity in the right forelimb. The filly also is toed in, a common finding in horses with this type of conformation. Another common finding is lateral deviation or bowing of the elbow, prompting clinical suspicion that a deformity also exists at this joint.

studies, a relationship between offset knees and carpal lameness was not found, but horses with this conformational abnormality were at risk for fetlock lameness.16,17 Toed-in conformation, or internal rotation of the distal extremity, exists alone or in combination with abnormalities of stance (base narrow or base wide), other conformational faults such as carpus varus and offset knees, and being wide in the chest (see Figure 4-16). Horses that are toed in usually wing out (paddle) (see Figure 4-13). Toed-in conformation is particularly undesirable in a trotter because of potential interference at speed. Toed-in conformation predisposes horses to lateral splints, lameness of the lateral aspect of the fetlock joint region (e.g., lateral branch suspensory desmitis), and OA of the interphalangeal joints. Horses that are toed in wear the outside aspect of the foot. Toed-out conformation, or external rotation of the distal extremity, is common and if mild may be considered normal or inconsequential (Figure 4-19). Mild toed-out conformation appears in 50% of STBs and is common behind in STBs and WBLs.10,12 It first develops in foals and, if pronounced, persists in the mature horse. In foals, toedout conformation often accompanies carpus valgus deformities but may result from external rotation primarily from the fetlock joint distally or, in more severe deformities, from further proximally (Figure 4-20). Mild toed-out conformation usually resolves as a foal matures and with corrective trimming. Toed-out conformation results in abnormal wear on the inside aspect of the foot. Horses tend



Chapter 4  Conformation and Lameness

25

Fig. 4-20  •  Thoroughbred foal with pronounced external rotation or toed-out left forelimb limb conformation. The deformity involves the entire limb, beginning well above the carpus.

Fig. 4-18  •  Dorsopalmar xeroradiograph of 3-year-old Standardbred colt with longitudinal fracture of the third metacarpal bone (small arrow). Medial is to the right. The lateral displacement (“step”) at the antebrachiocarpal joint (large arrow) gives the clinical appearance of an offset (bench) knee.

to wing in; if winging in is severe, particularly if accompanied by base-narrow conformation, it may interfere with the opposite forelimb (see Figure 4-13). Exostoses (splints) on the second metacarpal bone (McII) or McIII may develop, requiring protective boots to be worn during exercise. In STB pacers, interference injury occurs as high as the distal aspect of the radius.

Lateral Perspective

Fig. 4-19  •  Trotter showing inconsequential mild toed-out conformation. Toe weights often are used in trotters to balance gait and correct interference.

Horses camped out in front stand consistently with an entire forelimb ahead of the plumb line, but this conformation usually is a temporary problem with the horse’s stance and can be corrected by repositioning the horse, or it reflects pain caused by laminitis, for example. Camped under in front is unusual and usually also results from temporary malpositioning of the horse (Figure 4-21). If a horse prefers to stand camped under and is otherwise sound, however, this trait may be a sign of “extreme speed.”19 Back-at-the-knee or calf-knee (sheep-knee) conformation describes a concave dorsal aspect of the limb, with the carpus behind the plumb line (Figures 4-22 to 4-24). On radiographs of a normal carpus the proximal and distal rows of carpal bones are aligned in a proximal-to-distal direction, and the dorsal faces of these bones are parallel to the radius and the McIII (Figure 4-23, A). With back-atthe-knee conformation the proximal row of carpal bones is set back (Figure 4-23, B). Horses that stand back at the knee are considered predisposed to carpal injuries because of the natural tendency of the carpus to hyperextend (larger carpal angle) during fatigue. In our experience, TB racehorses are particularly at risk, despite limited contrary evidence (see page 16).14 While no associations were made between horses with back-at-the-knee conformation and lameness in recent studies in TBs and QHs, horses

26

PART I  Diagnosis of Lameness

A

B

Fig. 4-21  •  Diagram showing (A) camped-out in front and (B) campedunder in front conformation, both in relation to plumb lines.

A

Fig. 4-22  •  Thoroughbred yearling with back-at-the-knee (calf-knee) conformation most noticeable in the left forelimb. This conformational fault is undesirable, particularly in racing breeds.

B

Fig. 4-23  •  Lateromedial radiographs of the left carpi of two 2-year-old Thoroughbred racehorses. A, There is normal carpal conformation, and the proximal and distal rows of carpal bones are aligned and parallel to the radius and third metacarpal bone. B, In a horse with carpal lameness there is palmar deviation of the proximal row of carpal bones. This radiological appearance is typical of back-at-the-knee conformation.

included in those studies were elite, and any foals with obvious back-at-the-knee conformation may have been eliminated from the case population before the studies commenced.16,17 In a different study TB foals that were back-at-the-knee improved as they matured from 1, 2, and 3 years of age.15

In the STB, mild calf-knee conformation is common in pacers and acceptable, whereas in the trotter this defect is undesirable. In other breeds, mild calf-knee conformation may not directly lead to lameness. In young horses with lameness from unrelated sources such as osteochondrosis or fracture of the distal phalanx, back-at-the-knee



Chapter 4  Conformation and Lameness

27

Fig. 4-25  •  Older horse without obvious lameness with over-at-the-knee (bucked-knee) conformation.

Fig. 4-24  •  Clydesdale yearling with calf-knee conformation and clubfoot secondary to osteochondrosis of the shoulder joint. This conformation is primarily the result of chronic lameness, decreased weight bearing, and the development of a flexural deformity.

conformation and clubfoot (a small, upright foot) may accompany flexural deformity of the limb (see Figure 4-24). This deformity is a combination of contraction (clubfoot) and laxity (calf-knee) caused by chronic lameness and partial weight bearing and warrants a guarded prognosis. Over-at-the-knee, bucked-knee (knee-sprung), or hangingknee conformation describes a convex dorsal surface of the carpus, with the carpus in front of the plumb line (Figure 4-25). In young, untrained horses, bucked-knee conformation may be a predictor of lameness, but in mature horses it appears to be an acquired characteristic and occurs primarily in horses that jump. Older cross-country horses, steeplechasers, jumpers, or field hunters are prone to buckedknee conformation and often stand over at the knee with no obvious lameness. These horses may exhibit a tendency to buck forward to such an extent that they appear on the verge of collapse or prone to stumbling yet show good stability. Lame horses that stand over at the knee are often found to have pain in the proximal palmar metacarpal area or carpal sheath. Tied in below the knee (Figure 4-26) describes a distinct notch just distal to the accessory carpal bone on the palmar aspect of the limb. Normally, the McIII and the digital flexor tendons are in parallel alignment from the

a

b

A

B

Fig. 4-26  •  A, Diagrammatic representation of tied in below the knee. The dorsal-palmar length of a is less than b, giving the appearance that the digital flexor tendons run obliquely, proximally to enter the distal carpal region more dorsally than expected. B, A horse that is cut-out under the knee has a concave appearance of the dorsal aspect of the distal carpus and proximal metacarpal region (arrow).

PART I  Diagnosis of Lameness

28

accessory carpal bone to the proximal sesamoid bones. With tied-in conformation the digital flexor tendons appear to enter the carpus in a dorsoproximal direction. If the horse also is bucked kneed, the tied-in appearance is accentuated. Young horses are prone to superficial digital flexor tendonitis. In STBs this defect is worse for a pacer than a trotter. The junction of the carpus and McIII should be flat. Cut out under knee describes a notch under the dorsal surface of the carpus (see Figure 4-26). In horses with this defect, the McIII appears thin (dorsopalmar direction) and weak. Horses with this conformational abnormality also are often back at the knee, predisposing them to carpal and metacarpal problems. Some young racehorses, typically late yearlings or early 2-year-olds in training, appear to have distention of the middle carpal joint capsule or an unusually prominent distal radial epiphysis. These findings give the impression of an unusually large gap between these structures, described as “open at the knee.” The first author has not seen a correlation between this clinical observation and obvious radiological changes, although in young horses with this conformation the distal radial physis remains visible. Whether this conformation is relevant to lameness in young racehorses is debatable. Over at the fetlock usually is seen in young horses with flexural deformity of this joint (see Chapter 59). This conformational fault may persist in a mature horse, causing upright pasterns or knuckling of the fetlock joint. In some horses this condition causes a progressive, permanent deformity and severe lameness, whereas in others a dynamic, intermittent knuckling occurs and some of these horses remain surprisingly sound. Knuckling also may be a sequel to desmitis of the accessory ligament of the deep digital flexor tendon.

A

B

HINDLIMB CONFORMATION Lateral Perspective Hindlimb conformational faults generally are less numerous and problematic than those in the forelimb because of differences in weight distribution and center of gravity. Plumb lines also are useful in evaluating conformation of the hindlimbs with the horse standing squarely, loading all limbs (see Figure 4-11). Camped-out conformation is unusual and generally results from faulty positioning of the horse during the examination. Horses that are truly camped out usually have short strides and poor athletic ability. Camped under behind often is associated with sickle-hocked conformation but also appears in horses that are straight behind (Figures 4-27 and 4-28). Horses with this type of conformation often have short, choppy strides (Figure 4-29). A particularly severe conformational fault that leads directly to lameness is straight behind, otherwise called straight hocks or post (posty) leg. Horses that are straight behind have larger stifle and hock angles but smaller fetlock joint angles compared with ideal hindlimb conformation (see Figures 4-27 and 4-28). Straight-behind, sicklehocked, and in-at-the-hock conformation are the three most important hindlimb conformational faults, and all may lead directly to lameness. Horses that are straight behind often develop upward fixation of the patella, a condition seen most often in WBLs. Suspensory desmitis and fetlock OA also occur frequently. Horses with normal initial hindlimb conformation may become straight behind if they develop severe suspensory desmitis and lose support of the fetlock joint (see Chapter 72).

C

D

Fig. 4-27  •  Diagrammatic representation of conformational faults of the hindlimb from the lateral perspective. Compared with ideal conformation, horses with sickle-hocked conformation (A) have a concave dorsal surface of the limb with the distal extremity dorsal to the plumb line, but those that are straight behind (B) have large stifle and hock joint angles but smaller fetlock joint angles. Horses that are camped under (C) often are sickle hocked as well. Camped-out conformation (D) is unusual and most often results from faulty positioning of the horse.



Chapter 4  Conformation and Lameness

29

Fig. 4-28  •  Standardbred filly with straight hindlimb conformation and suspensory desmitis. Fig. 4-29  •  Horse with camped-under and mild sickle-hocked conformation, a combination leading to a short, choppy gait.

Fig. 4-30  •  This 4-year-old Standardbred has sickle-hocked conformation and has developed curb, which has been treated by freeze-firing, resulting in white marks on the plantar aspect of the hocks.

Sickle-hocked conformation is one of the most common conformational faults, and it leads directly to lameness of the tarsus and plantar soft tissues. Horses that are sickle hocked stand with the lower hindlimb well ahead of the plumb line, with an exaggerated concave dorsal surface of the hindlimb (resembling a sickle), creating a smaller than normal hock angle (see Figures 4-27, 4-29, 4-30, and 4-31). This type of conformation is often called curby conformation because horses frequently develop curb (see Chapter 78). Sickle-hocked conformation concentrates load in the distal, plantar aspect of the hock, predisposing to curb and to distal hock joint pain. In a recent study evaluating tarsal angles and joint kinematics and kinetics, horses with large hock angles (straighter behind) had less absorbed concussion during impact, smaller vertical impulse, and less extensor movement, characteristics thought to predispose these horses to OA.20 One of us (MWR) feels results of this study could be interpreted differently, since clinical experience contradicts this finding; horses with larger hock angles are at less risk of the development of OA of the distal hock joints and less absorbed concussion by the tarsus may make other structures such as the suspensory ligament at risk of injury. However, smaller net movement in horses with larger hock angles may be protective for the development of plantar tarsal

30

PART I  Diagnosis of Lameness

A

B

C

D

E

Fig. 4-31  •  Hindlimb conformational abnormalities viewed from the rear. A, Cow-hocked conformation is a common fault characterized by external rotation of the limb, usually without angular deformity, causing the hocks to be too close together. Mild external rotation of the hindlimbs is common and does not appear to cause lameness. B, Cowhocked, base-narrow conformation. C, Base-narrow conformation. D, Base-wide conformation is uncommon. E, Bowlegged conformation is uncommon and undesirable.

conditions such as curb, a finding that correlates well with my clinical impressions.20 In foals with incomplete or delayed ossification of the tarsal bones, marked sicklehocked conformation may occur (see Chapters 44 and 128). Sickle-hocked conformation is undesirable, particularly in racing breeds, but if mild is not detrimental. In STB pacers, some prefer a mild degree of sickle-hocked conformation because horses can extend the hindlimbs farther forward without risk of interference. In STB trotters the condition often predisposes to distal hock joint pain and curb, but these horses tend to be fast, although unsound. In Western reining horses, sickle-hocked horses may be better able to perform sliding stops.

Rear Perspective

A majority of STB and WBL horses toe out behind, which should be considered normal. Horses with mild external rotation of the distal extremity are said to be toed out and usually also have external rotation of hocks, causing the points of the hocks to be closer than normal. This fault is called cow-hocked conformation and is a rotational change of the hindlimb (Figure 4-31). Cow-hocked conformation occurs in combination with base-wide or base-narrow deformities or independently. Cow-hocked and base-narrow conformation is most common. Base-wide and basenarrow conformation may occur without cow-hocked conformation. These conformational faults seldom lead to lameness but have a substantial effect on gait in some horses. Horses that are base narrow travel closely behind, particularly at a walk. Some travel closely at a trot, pace, or gallop, whereas others seem to widen out when going faster, thus avoiding interference. Those that travel closely at speed often interfere, causing injury to the medial aspect of the contralateral hindlimb.

Fig. 4-32  •  Mature Standardbred racehorse with in-at-the-hock (tarsus valgus) conformation. This conformational abnormality is characterized by an angular deformity as opposed to the rotational deformity seen in cowhocked conformation. The characteristic white marks were produced by cryotherapy for treatment of bilateral curb.

Chapter 4  Conformation and Lameness



Bowlegged hindlimb conformation, in which the point of both hocks is truly outside the plumb line, is uncommon (see Figure 4-31). Occasionally horses that are base narrow appear to be bowlegged. Unilateral bowlegged conformation occurs in foals born with windswept deformity or in those with tarsal varus deformity. Bilateral tarsal varus deformity is unusual. In at the hock or tarsus valgus is an angular deformity (see Figure 4-32). The deformity can be corrected in foals. If it persists in a mature horse, particularly a racehorse with other conformational abnormalities, such as sickle hocks, abnormal forces or load occur in the tarsal region, predisposing the horse to distal hock joint pain, curb, and proximal metatarsal lameness. Horses can be toed in or toed out behind, but in general the conformational abnormality starts above the fetlock joint, causing the lower limb abnormality to be linked with the upper limb. Thus a horse that is toed in generally is bowlegged, and one that is toed out is cow hocked. In some foals, however, fetlock varus occurs independent of upper limb conformational abnormalities. This abnormality usually appears in windswept foals in which upper limb deformities have resolved, leaving a fetlock varus. This is an angular deformity, but with abnormal hoof wear, toed-in conformation can develop. Fetlock varus and the resulting toed-in conformational defect may cause OA of the fetlock and interphalangeal joints and can be career-limiting.

CONFORMATION OF THE DIGIT More detailed aspects of conformation of the foot and limb flight characteristics are discussed in Chapters 5, 7, and 27. Many of the changes in hoof growth or conformational changes in the hoof are the result of wear, shoeing, and exercise demands of training and performance and often are not present in a young horse.

A

B

31

The pastern angle has traditionally been thought to be similar to the angle of the shoulder (see Figure 4-8). However, in the recent TB study front pastern angle was only mildly correlated to the scapular spine angle, and there was variability.15 Variability was likely from shoeing and lowering of the heel. There was a good correlation between pastern and hoof angles.15 The foot-pastern axis should be straight. The pastern should be neither excessively sloped (low angle) nor upright (high angle). The angle of the pastern is important in determining the amount of load on the lower limb structures. In general, the more upright the pastern (steeper pastern angle), the shorter the stride and vice versa. Horses with upright pasterns appear to be prone to foot lameness and perhaps superficial digital flexor tendonitis. Those with long, sloping pasterns may be at risk to develop OA of the fetlock joint and proximal phalangeal fractures. Horses with short, upright pasterns but relatively normal hoof angles have a broken foot-pastern axis—the foot axis is lower than the pastern axis—and are at risk for developing foot lameness (Figure 4-33). Horses with broken back foot–pastern axis often have underrun heels and other hoof abnormalities and should be evaluated for corrective trimming if lame. If the pastern axis is lower than the foot axis (broken forward foot–pastern axis), called coon-footed, it causes undue strain on the soft tissue structures supporting the fetlock joint. This type of conformation may result from severe suspensory desmitis and loss of support of the fetlock joint. Pastern length is important and usually is related to pastern angle. Horses with long pasterns commonly have more slope or lower pastern angles. The plumb line should drop approximately 5 cm behind the heel in a well-conformed horse. In horses with long, sloping, and weak pasterns, the line drops more than 5 cm behind the heel. Those with short pasterns usually have more upright pasterns, and the plumb line drops through the foot. A variety of pastern lengths and angles occur, but the pastern length should be in proportion to the overall length of the limb.

C

Fig. 4-33  •  Diagrammatic representation of ideal pastern and foot conformation and the concept of a broken pastern-foot axis. Ideally the foot and pastern angles (A) should be identical to allow full and even weight bearing on all aspects of the foot. A broken foot axis (B) occurs when pastern angle is more upright than that of the foot or vice versa (C). In both latter situations, uneven load distribution on the foot or soft tissue structures may cause lameness.

32

PART I  Diagnosis of Lameness

Viewed from the front, the plumb line may divide the pastern and foot asymmetrically with more pastern and foot laterally, which often is associated with some degree of distortion of the hoof capsule, with a steeper medial wall and some flaring laterally. This results in asymmetrical loading of the distal limb joints and may predispose to lameness. Buttress foot is an acquired firm bulge or swelling at and proximal to the dorsal aspect of the coronary band and usually reflects OA of the distal interphalangeal joint (sometimes called pyramidal disease). Bull-nose foot conformation, an abnormal convex dorsal hoof wall, is uncommon but is occasionally seen in a hind foot (Figure 4-34). It is possible to cause this abnormal hoof conformation by incorrect trimming of the dorsal hoof wall, but in most horses it is caused by faulty hoof growth. One of us (MWR) has seen this type of abnormal hind foot conformation most commonly in the TB racehorse, and it is possible there may be a relationship between bull-nose hoof conformation and lameness of the digit or other areas of the distal aspect of the hindlimb. There may be a relationship between bull-nose foot conformation and long, weak pasterns (see Figure 4-34).

Fig. 4-34  •  Bull-nose foot conformation in a 3-year-old Thoroughbred racehorse that developed a medial condylar fracture of the distal aspect of the third metatarsal bone requiring surgical repair. The relationship between poor hoof conformation and lameness is unknown, but in this horse long, weak pasterns are seen and the combination of conformational faults may predispose horses to injury.

Chapter

5 

Observation: Symmetry and Posture Mike W. Ross

Assessments of symmetry and posture are important aspects of a lameness examination. Comparison between the normal and abnormal sides facilitates identification of abnormalities, unless the condition is bilateral so that no recognizable differences exist between the left and right limbs. The horse should be standing squarely on a flat surface in a quiet, insect-free environment. Horses with severe lameness often are reluctant to stand correctly, but information gained about symmetry and posture of severely lame horses is valuable. The veterinarian should look carefully at size, shape, contour, heights, and widths and compare with the opposite side.

FORELIMB SYMMETRY Muscle Atrophy

The symmetry of skeletal muscle in the forearm, pectoral, and cervical areas should be assessed. Muscle atrophy that occurs in horses with chronic lameness conditions is called disuse atrophy and in those with neurological disease is called neurogenic atrophy. Horses with muscle atrophy and lower motor neuron disease (see Chapter 11) may be lame, sometimes as a result of muscle pain or nerve root pain,

complicating differentiation between these causes of muscle atrophy. In most but not all horses with neurogenic atrophy, other clinical signs suggestive of neurological disease may be present. Horses with disuse atrophy resulting from chronic lameness usually have generalized atrophy of the ipsilateral forelimb. Muscle loss usually is not pronounced but involves the forearm (extensors are most commonly affected), triceps, and shoulder muscles. Shoulder muscle atrophy involving the infraspinatus and supraspinatus muscles generally is not pronounced, and lateral subluxation of the shoulder joint during weight bearing is not present (see Chapter 40). Development of disuse atrophy resulting from chronic lameness generally takes weeks to months unless severe lameness exists. In horses with severe or non–weightbearing lameness, atrophy may develop within 10 to 14 days. In horses with severe forelimb lameness, carpal contraction (flexural deformity of the carpus) may occur simultaneously with muscle atrophy. The most common causes of carpal contraction because of ipsilateral forelimb lameness are olecranon fracture and other elbow lameness, but carpal contraction may occur in horses with severe shoulder or even lower limb lameness. Atrophy of the triceps muscles usually is recognized before other muscle atrophy in severely lame horses. Horses with neurogenic atrophy may have profound atrophy of one or more muscles in the forearm, pectoral, or cervical regions. Atrophy often is much more pronounced than expected based on the degree of lameness, prompting suspicion of neurological disease. Pronounced, unilateral pectoral or triceps atrophy with mild atrophy of the forearm muscles suggests neurological disease. Severe atrophy localized to the infraspinatus or supraspinatus muscles without subluxation of the shoulder joint usually results from injury of the suprascapular nerve caused by



Chapter 5  Observation: Symmetry and Posture

external trauma. Atrophy and subluxation of the shoulder joint is associated with injury of the brachial plexus or nerve roots. Other muscles may also show atrophy. Localized muscle atrophy or fibrosis occurs in horses with previous injury and subsequent scar tissue formation within muscle bellies. This condition is more common in the hindlimb but occasionally occurs in the forelimb.

Swelling

Swelling, a common sign of inflammation, often causes asymmetry. The presence of swelling and heat should alert the lameness diagnostician to the possibility of an infectious process and may lead to additional examinations such as assessment of body temperature and the acquisition of laboratory data. Swelling within a joint capsule caused by excess joint fluid, effusion, is a general reaction of the joint to several traumatic or degenerative processes. Edema, cellulitis (lymphangitis), bleeding, and fibrosis can cause soft tissue swelling. Underlying bony enlargement can mimic soft tissue swelling, particularly in older horses with advanced osteoarthritis. Some swellings are clinically innocuous, such as mild distention of a digital flexor tendon sheath (so-called “windgalls” or “wind puffs”), but a recent change in size, local heat, or marked left-right asymmetry should alert the clinician to a possible problem. Occasionally a well-circumscribed tense spherical swelling is seen palmar to the neurovascular bundle on the side of the fetlock. These synovium-filled masses are usually incidental findings of no clinical significance. Edema usually signals acute inflammation, and pits (a distinct impression is visible) when compressed by digital palpation (pitting edema). Horses develop edema around and often distal to the site of inflammation. In some horses, especially racehorses left unbandaged when accustomed to being bandaged, benign mild-to-moderate edema of the distal extremities develops. This process is called “stocking-up” and should not be misinterpreted as a pathological process. In these horses the edematous area is not painful and usually does not pit, and the horse is not lame. Edema in these horses can complicate lameness examination because it is sometimes difficult to palpate underlying structures and to perform diagnostic analgesia. Cellulitis describes infection within the tissue planes of the distal extremities (see Chapter 14) and is sometimes called lymphangitis. Lymphangitis, by definition, is inflammation of the lymphatic circulation of the limb, but the conditions are similar and the terms are used interchangeably. Swelling is firm, warm, and painful, and lameness is often pronounced. “Stovepipe” swelling describes this condition (“the horse is all stoved-up”). Horses generally show systemic signs such as fever and elevated white blood cell count. Cellulitis usually results from small puncture wounds that may be difficult to discover or occurs after articular, periarticular, or subcutaneous injections. Infection develops in subcutaneous tissues or deeper in the dense fascial planes and can be difficult to eradicate. Blunt trauma or fractures may cause bleeding within tissue planes. Severe lameness and swelling accompany fractures of the scapula and humerus, because large vessels are nearby. Bleeding may be severe and cause a decrease in plasma protein and packed blood cell volume values. In horses with fractures located more distally in the limb, swelling is less pronounced but still prominent. The most

33

likely location of injury is the swollen area, but swelling may occur distal to the site of injury because of venous and lymphatic congestion. Fibrosis or scar tissue formation as the result of previous cellulitis or trauma causes asymmetry of the distal extremities but may not be the source of the current lameness. The veterinarian should avoid overinterpreting areas of scar tissue formation unless evidence of recrudescent inflammation exists. Horses may have scars caused by previous application of counterirritants or from healed wounds, leaving large, painless, and thus benign blemishes. Scars from previous surgical procedures, sometimes recognized by small areas of white hair accumulation, should be noted but may have no bearing on the current problem. Previous scars may have more relevance during prepurchase examinations. Bony swelling is a common cause of asymmetry. Proliferative change results in periosteal or periarticular new bone formation and accompanies myriad problems in the distal extremities. Bony changes may be active, causing the current lameness problem, or old and inactive, causing few or no clinical signs. For example, old inactive bony swelling of the shin or osselets (bony and fibrous swelling of the fetlock joint) may be prominent in ex-racehorses but may have little to no relevance to current lameness.

Angular Deformity

Angular limb deformities in young horses are common, are sometimes associated with lameness or other developmental orthopedic disease, and are discussed elsewhere (see Chapter 58). Abnormalities of conformation should be noted but may have little relevance to the current lameness problem (see Chapter 4). Horses younger than 2 years of age with severe forelimb lameness of several months’ duration may develop contralateral varus deformity originating from the carpus or elbow joints. Horses with severe lameness usually caused by trauma may have luxation or subluxation of joints as a result of collateral ligament injury or fractures and may have an acute change in limb angulation. Angular deviations of limbs are unusual in older horses and generally signal severe injury. Visual examination should be followed by careful palpation during which varus and valgus stress is applied to joints. Stress radiographs can be useful to determine collateral ligament integrity.

Foot Size

Ideally both front feet should be identical in size and shape, or nearly so, and any asymmetry should be noted. Horses with chronic lameness may have disparity in foot size, usually with the smaller foot being ipsilateral to lameness. The small foot often is contracted and more upright (Figure 5-1). Chronic reduction in weight bearing results in foot size disparity in some, but not all, horses. Mild disparity in foot size is a normal finding in some horses. Mild clubfoot conformation, acquired from previous flexural deformity, may be present incidentally in adult horses. Previous lameness may have caused contraction of the foot but has since resolved, resulting in disparity in foot size and shape but no residual lameness. In these horses it would be a mistake to assume current lameness is originating from the foot without confirmation using diagnostic analgesia. Clubfoot conformation appears to be better

PART I  Diagnosis of Lameness

34

A

Fig. 5-2  •  Standardbred racehorse with severe suspensory desmitis and a “dropped fetlock.” The level of the right front fetlock joint is lower than that of the left front, caused by chronic, severe desmitis. Similar clinical signs and severe lameness appear in horses with acute traumatic disruption of the suspensory apparatus.

B Fig. 5-1  •  A horse with disparity in front foot size caused by chronic lameness. The right forelimb foot is smaller compared with the normal left forelimb foot when viewed from the front (A) and more upright when viewed from the side (B).

tolerated in Thoroughbred (TB) than in Standardbred (STB) racehorses.

Fetlock Height

Fetlock position should be assessed in the standing horse and during movement. In a standing horse, fetlock height should be symmetrical, assuming the horse is loading the limbs equally. Horses with severe lameness commonly “point” or hold the limb in front of the opposite forelimb, thus taking weight off the limb. This standing posture obviously causes disparity in fetlock height but should be carefully interpreted. Loss of support of a fetlock in the standing horse causes the affected fetlock to drop and occurs most commonly with acute, traumatic disruption of the suspensory apparatus in racehorses but also appears with chronic, active desmitis (Figure 5-2). Severe superficial digital flexor tendonitis or lacerations resulting in fiber

damage of the deep or superficial digital flexor tendons can cause similar clinical signs. In horses with mild flexural deformity of the metacarpophalangeal joint, dynamic knuckling (buckling forward, flexion) of the fetlock joint may occur in the standing position (Figure 5-3). Joint position usually returns to normal during movement. In horses with severe flexural deformity, normal fetlock position is never achieved. Knuckling of the fetlock also may result from desmitis of the accessory ligament of the deep digital flexor tendon.

Scapular Height

Disparity in scapular height is a rare clinical sign in a lame horse. The veterinarian must stand behind and above the horse to observe scapular height. The horse’s mane may obscure observation from a distance, requiring closer examination by palpation. Traumatic or neurological conditions affect scapular height, causing either injury or dysfunction of the serratus ventralis muscle, respectively. With both conditions the dorsal aspect of the scapula is higher on the affected side. The veterinarian may place pieces of white tape or other suitable markers on both sides of the horse and stand back to compare height or may use two assistants to point to the locations. Horses may have disparity in scapular height unrelated to the current lameness condition if there has been resolution of the original injury or neurological problem. Care must be taken to differentiate between genuine differences in the height of each scapula and asymmetrical musculature,



Chapter 5  Observation: Symmetry and Posture

35

Fig. 5-4  •  Three-year-old Thoroughbred filly with subtle disparity in tubera sacrale height. The left tuber sacrale is slightly lower (arrow) than the right, caused by a fracture at the base of the tuber sacrale. This clinical finding can easily be missed or confused with mild muscle atrophy. Fig. 5-3  •  Knuckling forward of the right front fetlock joint occurs in a standing position in this horse with mild flexural deformity of the metacarpophalangeal joint. This dynamic instability abates somewhat when the horse moves, but the left front fetlock also is straight, indicating the presence of bilateral flexural deformity.

which occurs much more commonly and may be an incidental observation. Horses with disparity in scapular height or asymmetrical muscle development may have problems with saddle fit.

HINDLIMB SYMMETRY Muscle Atrophy

Asymmetry of bone and muscle mass in the hindlimbs and pelvis is a common clinical sign but must be differentiated carefully. The horse should stand squarely on a flat, even surface. The clinician must determine whether asymmetry exists, and if so, if the problem involves muscle, bone, or a combination of the tissues. Muscle atrophy is most common and, if unilateral muscle atrophy exists, easily can be confused with bony asymmetry caused by pelvic fractures or asymmetry of the tubera sacrale. Disuse and neurogenic muscle atrophy occur in the hindlimb. Horses with chronic hindlimb lameness develop ipsilateral gluteal muscle atrophy, but asymmetry may be subtle. Mild muscle atrophy usually first appears just lateral to a tuber sacrale. The veterinarian should differentiate muscle atrophy from disparity in height of the tubera sacrale (Figure 5-4). Recognition of muscle atrophy helps determine the lame leg and provides some information about the duration of the problem. Severe muscle atrophy develops in horses with long-standing, severe lameness or in those with neurological disease (Figure 5-5). In horses with neurogenic atrophy of the gluteal muscles the degree of muscle loss is inappropriately severe compared

Fig. 5-5  •  A 4-year-old Standardbred with severe left gluteal atrophy caused by neurological disease. The presumptive clinical diagnosis was equine protozoal myelitis.

with observed lameness. Neurological signs such as weakness and proprioceptive deficits usually appear in horses with neurogenic atrophy, but early in the course of diseases such as equine protozoal myelitis (EPM) the only observable signs may be muscle atrophy and mild lameness.

36

References on page 1256

PART I  Diagnosis of Lameness

Selective atrophy of individual muscles or muscle groups occurs in horses with neurological disease or injuries causing focal muscle loss and scarring. Horses with trauma involving fracture of the tubera ischii may develop focal muscle loss of the semitendinosus or semimembranosus muscles. A depression, sometimes subtle, resulting from localized muscle atrophy replaces initial swelling of the point of the rump. Horses with fibrotic myopathy, which in most horses is believed to result from injury and scarring of the semitendinosus muscle, usually have palpable scars or defects of the caudal thigh muscles. Degenerative neuropathy of the nerves supplying the distal aspect of the semitendinosus muscle also may cause fibrotic myopathy1 (see Chapter 48).

horses hematomas can be confused with severe femo­ ropatellar effusion (Figure 5-7). Excessive bleeding from subcutaneous vessels also may involve the ventral, lateral abdominal region. In horses with stifle hematoma, lameness may not be as prominent as expected, and swelling

Swelling

Swelling is especially important in horses with acute, severe lameness when the clinician must differentiate between catastrophic injury, such as pelvic or long bone fracture, and more common conditions, such as cellulitis. Horses with pelvic fractures may develop mild swelling in the thigh, but swelling is not prominent in most horses. In horses with fracture of a tuber coxae or ilial wing or shaft, mild swelling may develop distally but usually is not prominent. Inappropriate lameness and lack of swelling should prompt the clinician to perform a rectal examination, checking for internal asymmetry or crepitus. Horses with femoral fractures develop acute, severe swelling of the thigh, accompanied by severe lameness, instability, and often crepitus (Figure 5-6). Horses may develop severe swelling of the stifle and thigh resulting from trauma and secondary bleeding. Large stifle hematomas resemble the swelling in horses with femoral fractures, and in some

Fig. 5-6  •  A Thoroughbred broodmare with severe lameness and swelling of the left thigh caused by a comminuted femoral fracture.

Fig. 5-7  •  Moderate, fluctuant soft tissue swelling over the stifle caused by subcutaneous bleeding (hematoma). In this situation, swelling is much more pronounced than expected for the observed degree of lameness.



Chapter 5  Observation: Symmetry and Posture

37

fluctuates, which is useful in differentiating this cause of lameness from femoral fractures. Generalized, diffuse soft tissue swelling appears in horses with cellulitis or lymphangitis in the hindlimb (Figure 5-8). Horses that negotiate fences such as event and timber horses are at risk for stifleregion trauma and swelling.

rotation occur in horses with fracture of the wing of the ilium caudal to the tuber coxae without an obvious change in size or shape of the tuber coxae. However, with a partial fracture of the ventral aspect of the tuber coxae, there is a change in its shape without displacement of the dorsal aspect of the bone.

Bony Asymmetry

Tubera Sacrale

Comparison of the height of the tubera coxae is important to determine the nature and extent of pelvic bony injury (Figure 5-9). Two assistants, one on each side of the horse, may point to the dorsal aspect of the tubera coxae, or the veterinarian may use temporary markers to compare the height. Determining the height of the tubera sacrale may be difficult and requires careful palpation to differentiate bone, ligament, and muscle asymmetry. Accurate deter­ mination may be possible only by ultrasonography. Estimating the midline-to-lateral pelvic width also aids in diagnosing acute or chronic pelvic fractures.

Tubera Coxae

Asymmetry in height of the tubera coxae accompanies many different pelvic fractures. The most common fracture involves the tuber coxae itself, often called knocked-down hip. Marked ventral and medial displacement of the fracture fragment occurs because of muscle attachment to the bony prominence. The veterinarian also must palpate the actual shape of the tuber coxae, because ventral displacement occurs with other pelvic injuries. Displacement and

Fig. 5-8  •  Soft tissue swelling caused by cellulitis. Firm, painful swelling appears in the entire limb.

The term hunter’s bump describes the prominence of the tubera sacrale. This finding may reflect the horse’s conformation, poorly developed surrounding musculature, or a change in position of one or both tubera sacrale. Increase or decrease in size of the overlying dorsal sacroiliac ligament also results in apparent asymmetry. Many clinically normal horses have slight apparent asymmetry of the tubera sacrale. Asymmetry in height of the tubera sacrale occurs in horses with acute or chronic sacroiliac joint disruption (Figure 5-10). In horses with acute fractures of the base of the tubera sacrale, the affected side is lower2 (see Chapters 49 and 50). Ultrasonography and nuclear scintigraphy may help identify the cause of asymmetry.

Midline-to-Lateral Pelvic Width

A change in the relative width of each hemipelvis is a subtle but important clinical sign of pelvic injury. In most horses with pelvic fractures, the injured side is narrower than the normal side. Overriding and displacement of fracture fragments result in compression on the injured side.

Fig. 5-9  •  A horse that is well positioned for determination of tubera coxae height and the midline-to-lateral pelvic width (X, Y). In a normal horse, X = Y.

38

PART I  Diagnosis of Lameness

Fig. 5-10  •  Asymmetry of the tubera sacrale. The left tuber sacrale (arrow) is higher than the right. This horse has chronic left sacroiliac subluxation.

Swelling over the Greater Trochanter

Mild swelling over the lateral aspect of the coxofemoral joint may be a subtle clinical sign of acetabular or proximal femoral fractures. When standing behind the horse, the veterinarian should carefully observe for enlargement over the affected hip joint. This clinical sign usually is not noticeable initially, but soft tissue enlargement is visible within 2 to 3 weeks after intraarticular fracture. The groove between the greater trochanter and the biceps femoris muscle should be compared carefully; usually a slight bulge or subtle enlargement on the affected side is visible.

Crepitus

Fig. 5-11  •  A horse with partial disruption of the left gastrocnemius. An injury to the origin of the lateral head of the gastrocnemius muscle in this horse caused an unusual gait deficit, lameness, and mild distal displacement (drop) of the hock and fetlock.

Bone-on-bone grating is a valuable clinical sign, particularly in horses with pelvic injury. Crepitus can be heard (with or without a stethoscope) or felt (external or rectal palpation) and most often is caused by movement of bone fragments in horses with displaced fractures (see Chapter 6). In horses with pelvic fractures, crepitus usually is not observed for several days to weeks after injury because muscle tone and fracture hematoma apparently stabilize fracture fragments and delay onset. Crepitus also can be felt or heard in horses with end-stage osteoarthritis.

Calcaneus

The points of the hock should be of equal height when observed from the side or from behind. There is dramatic lowering of the point of the hock with complete disruption of the common calcaneal tendon or gastrocnemius tendon alone. Partial injury of the gastrocnemius muscle origin, the musculotendonous junction, or the tendon itself causes varying degrees of asymmetry in height of the point of the hock, both in a standing horse and during movement.3 Other gait abnormalities such as unusual rotation or instability of the limb usually are present (Figure 5-11). The point of the hock is elevated in horses with severe pelvic fractures involving the acetabulum, luxation of the coxofemoral joint, and some femoral fractures (Figure 5-12). Evaluating elevation is difficult because horses with severe lameness usually cannot bear weight, causing a dramatic alteration in limb position. However, in horses with true elevation in the point of the hock, the hock is extended,

Fig. 5-12  •  A horse with a comminuted fracture of the left femur. The point of the left hock is higher than that of the right as a result of overriding of fracture fragments and muscle contraction, effectively shortening the limb.



Chapter 5  Observation: Symmetry and Posture

39

apparatus. A change in posture usually means a part of the reciprocal apparatus is broken.

FORELIMB POSTURE Pointing

Horses that are severely lame often point or hold the affected forelimb ahead of the unaffected forelimb, or the least affected forelimb in horses with bilateral pain. These horses usually are severely lame at a walk. Horses with severe, bilateral forelimb lameness caused by laminitis may stand camped out in front, attempting to point with both forelimbs simultaneously. However, pointing is not synonymous with the presence of pain or lameness or its degree. Some horses prefer to point one forelimb or another and walk and trot normally. In general, pointing is unusual and often signals resting pain or subtle pain relieved by adopting this posture. Some horses stack bedding under the heel of one or both front feet to stand in a toe-down position, indicating a degree of unilateral or bilateral foot pain. These horses often are not as lame as expected based on the degree of postural change seen at rest. Alternatively a horse may stand with its hindquarters “sitting” on a manger partially to unload the front feet.

Fig. 5-13  •  Warmblood gelding with chronic, severe, bilateral hindlimb suspensory desmitis causing noticeable fetlock drop in the left hindlimb.

whereas with most non–weight-bearing conditions, the hock is flexed.

Fetlock Height

Assessment of fetlock position is as important in the hindlimb as in the forelimb. Horses with excessively straight hindlimb conformation (straight hocks) may have more obvious excursion of the fetlock (fetlock drop) while moving or shifting position during standing. Pathological fetlock drop generally accompanies suspensory desmitis (Figure 5-13) but also occurs with partial disruption of the gastrocnemius and other ligamentous and tendonous injuries.

POSTURE Body posture provides important clues to the source of lameness, but some abnormalities may be missed unless the horse is observed over long periods. Normal horses tend to rest one hindlimb and may alternate between limbs. Resting a forelimb is uncommon but does occur. Distractions in the environment may make a horse stand normally despite pain. However, abnormal posture because of mechanical or neurological dysfunction usually is evident. The horse has a well-developed stay apparatus in both the forelimbs and hindlimbs.4 It is assumed that the main purpose of the stay apparatus is to allow the horse to remain standing for long periods. The stay apparatus in the hindlimbs is better developed than in the forelimbs and includes ligamentous and tendonous structures dictating predictable movement of joints in the limb. If intact, the hindlimb stay apparatus demands reciprocal movement of the hock and stifle and often is called the reciprocal

Treading

Constant shifting of weight from one forelimb to the other may indicate bilateral forelimb lameness. Laminitis, severe soft tissue injuries such as tendonitis or suspensory desmitis, or severe osteoarthritis may cause treading. Horses with chronic, severe unilateral forelimb lameness often stand with little weight on the affected limb, overload the unaffected limb, and seldom tread. The development of treading in such circumstances is an ominous sign because the horse now is trying to shift weight from the previously unaffected limb, probably because of laminitis.

Buckling Forward at the Knee

Horses with bucked-knee or over-at-the-knee conformation may buckle forward at the knee while standing. In clinically normal older field hunters or other heavily used riding horses with bilateral over-at-the-knee conformation, this may be particularly obvious. The carpus is locked in extension primarily by the action of the extensor muscles. Neurological disease (e.g., EPM) affecting forelimb extensor muscles is a rare cause of buckling forward at the knee, both at rest and during movement. Specific injury of the distal aspect of the radial nerve causes similar clinical signs. In foals, rupture of the common digital extensor tendon or other extensor tendons may cause this posture (see Chapters 77 and 128).

Dropped Elbow

A dropped elbow results from failure of the triceps apparatus to maintain elbow extension (Figure 5-14) and usually results from fracture of the olecranon process. It also may result from injury to the radial nerve or brachial plexus. Similar clinical signs appear in horses with lesions of the nerve roots (neuritis, radiculopathy) or nerve cell bodies in the cervical intumescence, usually the result of lower motor neuron disease. A most unusual cause of this posture appears in horses with root signature (see the section on neck pain).

40

PART I  Diagnosis of Lameness

Fig. 5-15  •  Forelimb posture in a foal with osteomyelitis (scapula) and infectious arthritis (shoulder joint). With severe lameness of the  shoulder or bicipital bursa, horses are reluctant to stand or move  normally and often hold the limb caudally. This posture may be difficult  to differentiate from that seen with loss of the triceps apparatus (see  Figure 5-14).

Fig. 5-14  •  Classic forelimb posture most often called radial nerve paresis or paralysis. The horse cannot extend or fix the elbow, causing the appearance of dropped elbow. The inability to fix the elbow (loss of triceps apparatus) commonly occurs in horses with olecranon fractures.

Severe Lameness of the Shoulder Region Horses with severe shoulder pain may stand with the affected limb more caudal than usual (Figure 5-15) and often drag the limb with even the slightest movement. This posture is similar to dropped-elbow posture, but in horses with a dropped elbow the limb is held at, or even slightly cranial to, the expected position.

Neck Pain

Horses with neck pain often hold the head and neck lower than expected, at a level equal to or slightly lower than the withers (Figure 5-16). Historically some horses may be observed to get caught in this position. In horses with severe pain, muscle tremors or spasms are visible, especially when one approaches the horse or the horse moves; the horse may stand in a guarded position. The horse may be reluctant to turn or move and may be unable or unwilling to eat food from either the ground or an elevated position. An unusual but characteristic sign of neck pain is posturing of a single forelimb, usually on the side of the lesion. The limb is held extended or pointed in front of the other forelimb; rarely the limb is held in slight flexion (see Figure 53-10, A). This sign appears in dogs with cervical pain, most commonly from intervertebral disk disease, and is termed root signature.5,6 Pain associated with the nerve roots supplying the brachial plexus may be the cause. Such a

Fig. 5-16  •  Yearling Standardbred with neck pain on the left side showing typical stance and head and neck posture.



Video available at www.rossanddyson.com

Chapter 5  Observation: Symmetry and Posture

41

posture has also been seen in a horse with a mediastinal abscess. Some horses with cervical pain also have unilateral forelimb lameness.7

HINDLIMB POSTURE Resting a Hindlimb

Normally a horse rests one hindlimb or another, but immediate resting of a hindlimb after work, or a combination of resting of the hindlimb and trembling in the flank or stifle region, may indicate lameness. Resting of the hindlimb, particularly with trembling of the quadriceps muscles, often prompts handlers to erroneously assume the horse has stifle region pain. Horses with hindlimb pain from other locations will often assume this posture.

Abnormal Tail Position

Horses may carry the tail in an abnormal position during movement, often alerting an observer to possible hindlimb pain. The tail usually is carried away from the lame limb, but this finding is inconsistent. Horses seldom have an abnormal tail posture at rest unless the tail has been traumatized or set or there is severe hindlimb lameness.

External Rotation of the Hindlimb

Cow-hocked conformation is common, but unilateral external rotation may reflect pelvic injury (Figure 5-17). The veterinarian should verify this change in posture by moving and reevaluating the horse. Horses with pronounced unilateral external rotation usually have fractures of the acetabulum or the proximal aspect of the femur but may have nonarticular ilial shaft or wing fractures.

Hindlimb Varus Posture

Horses with chronic, severe unilateral hindlimb lameness may develop varus conformation of the contralateral limb (see Figure 5-17). This posture most often appears in foals and may develop 7 to 10 days after onset of lameness.

Treading

Constant shifting of weight between the hindlimbs, or treading, is an unusual clinical sign and usually indicates pronounced bilateral lameness. Horses with bilateral hindlimb laminitis or severe osteoarthritis of any joint may tread. Horses with chronic, severe unilateral hindlimb lameness can endure 4 to 6 weeks or more of weight bearing on the contralateral limb, but treading may be the earliest sign of traumatic laminitis in the supporting limb.

Camped Under

Camped under appears only in horses with bilateral hindlimb laminitis and is rare. Horses often tread and exhibit an unusual hindlimb gait (shortened caudal phase of the stride) when moved at a walk in hand. Pain arising from the thoracolumbar region may also result in a camped under posture.

Soft Tissue Injuries Altering Hindlimb Posture

Upward fixation of the patella causes rigid extension of all hindlimb joints in a standing horse (Figure 5-18). Patellar dysfunction resulting in fixed extension of the stifle also causes extension of the tarsus and lower limb joints because of the hindlimb reciprocal apparatus. The horse may

Fig. 5-17  •  A 2-year-old Belgian gelding with a fracture of the right femoral head and neck exhibits external rotation of the right hindlimb. Varus deformity of the left hindlimb also is visible.

maintain this posture during movement, or the posture may be intermittent and resolve when the horse is moved. Occasionally a horse with severe hindlimb lameness assumes a similar posture, apparently hanging the limb, but the limb is not locked in extension (Figure 5-19). Normal horses simply resting a hindlimb, or those with severe lameness, usually keep the sole facing the ground. Foals with unilateral or bilateral lateral patellar luxation have an unusual crouched hindlimb posture similar to femoral nerve paresis. The foal may have difficulty in rising if the condition is bilateral and severe or long-standing. Disruption of fibularis (peroneus) tertius allows the hock to extend abnormally during weight bearing. Foals occasionally stand excessively straight in the hock (extended) in the affected hindlimb. In foals the injury usually causes tearing at the origin of fibularis tertius from the distal aspect of the femur, but in adults injury may occur in the crus or at the distal aspect of the ligament as it courses over the hock. Swelling and excessive hock extension may occur with the latter injury (Figure 5-20). The diagnosis is confirmed by manipulation: the hock can be extended while the stifle is flexed. Rupture of the gastrocnemius tendon, or severe injury at any level of the muscle-tendon unit, causes mild or severe hindlimb postural change. During weight bearing,

42

PART I  Diagnosis of Lameness

Fig. 5-18  •  A horse with the classic posture seen with upward fixation of the patella. All joints are held in rigid extension, and the horse is forced to rest or bear weight on the dorsal aspect of the hoof wall.

the hock flexes excessively as the stifle is held in extension, so the point of the hock drops. This injury is called disruption of the caudal component of the reciprocal apparatus.8,9

Peripheral Nerve Deficits (see Chapter 11)

Sciatic nerve damage is rare. It occurs in foals as a result of injections into the thigh or rump or may occur transiently after injection of local anesthetic solution caudal to the coxofemoral joint. Horses with sciatic nerve damage support weight but appear to be crouched behind, because innervation to the gastrocnemius, flexor, and extensor muscles causes the hock to drop and fetlock to knuckle forward. Careful observation of stifle action and the ability to support weight are useful for attempting to differentiate this deficit from femoral nerve paresis. Horses with femoral nerve paresis also assume a crouched hindlimb posture but are unable to bear weight, and the stifle drops substantially (Figure 5-21). Because the reciprocal apparatus is intact, the inability to fix the stifle leads to hock flexion and knuckling (flexion) of the fetlock joint. If the condition is bilateral, the horse is unable to rise for more than a few seconds. Femoral nerve paresis may occur unilaterally or bilaterally after general anesthesia or may result from lower motor neuron disease or injury. Solitary tibial nerve injury is rare. Fibular (peroneal) nerve injury usually is recognized after general anesthesia and causes characteristic knuckling of the fetlock joint. Tibial nerve injury is differentiated from sciatic injury by lack of involvement of the fibular nerve, and thus normal

Fig. 5-19  •  Belgian gelding shown in Figure 5-17. This horse occasionally rested the left hindlimb in this extended position, similar to that of upward fixation of the patella. Most normal horses, or those with severe lameness, prefer to rest the limb with the sole facing the ground.

positioning of the hock, and from femoral nerve injury, because horses are able to support weight and fix the stifle. A rare polyneuropathy in Norwegian horses caused unilateral or bilateral knuckling of the hindlimbs, and in some horses paraplegia occurred as a result of peripheral injury of the sciatic nerves.10 A common epidemiological factor in all horses was the feeding of big bale silage or hay of poor quality.10 I have seen similar clinical signs in a Warmblood gelding, which developed acute, severe, bilateral hindlimb knuckling (at the fetlock) that resolved completely several days after onset. The cause in this horse was not determined.

Other Unusual Leg Positions

Horses with severe lameness occasionally rest a hindlimb back, forward, or abducted. Often these positions also are maintained during movement. Horses with caudal thigh or pelvic pain prefer to keep the affected hindlimb back, behind the unaffected limb. Horses with shivers may stand with the limb slightly abducted and more caudal than expected, with elevation of the tail head (see Chapter 48).

Stance in Horses with Pelvic Fractures and Conditions Affecting the Coxofemoral Region

Horses with pelvic fractures, in particular those involving the acetabulum, or other severe conditions involving the coxofemoral joint often stand with the limb slightly



Chapter 6  Palpation

43

Fig. 5-20  •  This Thoroughbred racehorse with fibularis tertius injury has swelling over the dorsal aspect of the hock (arrow) and straight-in-thehock conformation.

forward and often are reluctant to place the limb behind the unaffected limb, thus reducing the caudal phase of the stride at the walk. In addition, horses will often stand with the limb externally rotated, and in the rare instance there is coxofemoral luxation, the point of the hock of the affected limb will be slightly proximal to the contralateral point of the hock (see Figure 5-17). I find it interesting that children with infectious arthritis of the coxofemoral joint will often hold the affected hip in flexion, abduction, and external rotation,11,12 remarkably similar to those clinical

Fig. 5-21  •  Thoroughbred with transient, postanesthesia, unilateral (left hindlimb) femoral nerve paresis. The crouched posture of the left hindlimb includes flexion (knuckling) of the fetlock joint.

signs seen in the horse. Horses with pain in the medial thigh and groin area stand with the limb abducted and may travel in this manner. Adductor muscle damage, medial thigh abscessation, and scirrhous cord or other inguinal problems also cause this posture.

Chapter

6 

Palpation Mike W. Ross Palpation is an important part of a lameness examination. In some sports horses, it becomes more important because, for example, suspensory desmitis often is not associated with overt lameness but may compromise performance.

The veterinarian must develop a system to evaluate comprehensively all parts of the musculoskeletal system. I palpate in order each forelimb, the neck, the back, the pelvic regions, and then the hindlimbs. Each limb should be assessed when bearing weight and then again with the limb elevated from the ground. Deep palpation is used to describe direct, digital palpation, with the limb in an elevated position. If time permits, palpation should be completed before the horse is moved, because if the lame limb is identified first, the other limbs may be overlooked and compensatory problems may be missed. For example, in a Thoroughbred (TB) racehorse, superficial digital flexor (SDF) tendonitis is

44

PART I  Diagnosis of Lameness

a common compensatory problem caused by contralateral forelimb lameness resulting in overload. If a lame horse with left forelimb lameness is first examined while the horse is moving, and subsequent palpation of the limb reveals signs of possible fetlock osteoarthritis, mild swelling of the right forelimb SDF tendon (SDFT) may be missed. Comprehensive palpation may allow the clinician to make predictions about lameness, to “read” the horse. Palpation before exercise also facilitates identification of localized heat or swelling, because limb temperature increases with exercise, and swelling often decreases.

THE ART OF PALPATION The veterinarian should palpate and manipulate every possible anatomical structure, using the fingers and hands to push, prod, and feel. Interpretation of an abnormal response requires appreciation of the normal response. There are nerves beneath or adjacent to many structures, and direct pressure may elicit an apparently positive response. Such false-positive responses often occur during palpation of the origin of the suspensory ligament (SL) or the proximal sesamoid bones (PSBs). Care should be taken to apply pressure only in the desired location. During palpation of the PSBs, distal aspect of the SL, and digital flexor tendons, it is easy to apply pressure over the dorsal aspect of the third metacarpal bone (McIII), and a painful response may actually reflect sore shins. The clinician should look for signs of inflammation: heat, pain, redness, swelling, and loss of function. One side of the horse should be compared with the other, but it should be remembered that both sides may be abnormal. Heat is one of the earliest clinical signs to develop with articular or nonarticular problems and may be the only sign. Subchondral remodeling and sclerosis of the third carpal bone often cause lameness in young racehorses, but effusion of the middle carpal joint and a positive response to flexion are found inconsistently. Usually prominent heat is detectable on the dorsal aspect of the carpus. It is important to recognize normality. A normal horse may have disparity in foot temperature. Horses often have two or three cold feet, but the other foot or feet feel warm. A few hours later, feet that previously were cool may feel warm. Foot temperature often reflects variations in ambient temperature, and care must be taken not to overinterpret this normal finding. In general, palpation is done with the palm side of the hand, although the back of the hand may be more sensitive to detection of warmth. The veterinarian should assess the quality or strength of the digital pulse. In a normal horse, reliable detection of a digital pulse may be difficult, especially in cold weather or in horses with a thick hair coat. Increased or elevated digital pulse refers to the detection of increased strength (amplitude) or the bounding nature of the digital pulse. Inflammatory conditions in the foot or pastern region, such as abscesses, laminitis, hoof avulsions, or cracks, are the most common causes of increased digital pulse amplitude. Complete absence of hindlimb digital pulse may occur with aortoiliac thromboembolism or other vascular problems, but care should be taken when interpreting weak or near absent hindlimb digital pulses, because hindlimb digital pulses can be difficult to feel in normal horses.

Redness is difficult to perceive in the horse because of skin pigmentation, but in the foot, solar bruising or redness at the coronary band can be observed, especially in horses with nonpigmented feet. Swelling is often detected by observation, but subtle enlargement of structures such as the SL, or presence of effusion may be determined only by careful palpation. Loss of function of tissues and regions can be assessed during palpation. Manipulation, flexion, and extension of the joints or soft tissues provide a better idea of function or loss of function. Static flexion and extension determine the range of motion of a joint and the horse’s response to the procedure. Chronic osteoarthritis of the fetlock or carpal joints often results in reduced range of flexion. However, many horses in work but without lameness resent hard flexion of the lower limbs. Good correlation between a reduction in fetlock flexion range, lameness, and severity of osteoarthritis was found in TB racehorses.1 A reduction in fetlock flexibility in young Warmbloods may be a predictor of future lameness.2 The response to rotation of joints also should be assessed. Crepitus, the grating or crackling sound made by bone rubbing on bone, is an unusual and ominous clinical sign usually determined by palpation, although in horses with prominent osteoarthritis or fractures a grating sound may be heard. A stethoscope may be useful for detection of subtle crepitus. Other factors may confound the results of palpation. Clipped areas usually are warmer than an adjacent area with normal hair length. Blistering or freeze firing can cause localized pain for weeks after application, even if lameness has resolved. Any type of skin lesion, such as those found in horses with scratches or boot rubs, can cause extreme soreness to palpation but no signs of lameness. Some individual horses are more sensitive to palpation than others, and interpretation of apparent pain can be frustrating.

PALPATION OF THE FORELIMB Foot

The importance of the foot cannot be overemphasized, and it is for this reason that palpation of the forelimb begins here. The feet are included in evaluation of conformation, symmetry, and posture. Detailed static examination (examination at rest) of the foot must always be supplemented with, and correlated to, dynamic observations of foot flight and foot striking patterns. Some horses continually attempt to pick up the limb as the clinician tries to evaluate it with the horse in the standing position; it may be necessary to stroke the contralateral limb to divert attention. A hoof pick, wire brush, hoof knife, shoe-removing equipment, and hoof testers are required (Figure 6-1). The sole and frog and wall of the foot should be cleaned thoroughly. Removal of the shoe at this stage in the examination usually is indicated only if a subsolar abscess is suspected. The veterinarian should take care to preserve the hoof wall, and if it is cracked, protect it with tape. Foot and hoof balance are assessed by evaluating toe and heel length, hoof capsule conformation, condition and integrity, type of shoe and shoe position relative to the hoof capsule, hoof and pastern angle (axis), medial-tolateral hoof balance, coronary band conformation, and

References on page 1256



Chapter 6  Palpation

45

Fig. 6-1  •  Instruments needed to examine the hoof, remove a shoe without tearing the hoof wall, and prepare the hoof for radiographic examination. Shown are apron, rasp, shoe pullers, nail pullers, clinch tool, hoof knife, hammer and hoof pick, and wire brush.

distal interphalangeal (coffin) joint capsule distention and response to hoof testers. The coronary band should normally be parallel to the ground surface. Deviation from parallel often indicates mediolateral foot imbalance (Figure 6-2). Medial and lateral wall lengths should be assessed while the horse is standing and again with the limb off the ground, with the foot viewed from palmar to dorsal along the solar aspect. The limb is lifted and held in neutral position so the solar surface is perpendicular to the ground. Sheared and underrun heels are commonly associated with lameness (Figure 6-3). Deformation of the hoof capsule is not necessarily a cause of lameness. Many horses with proximal displacement of the medial heel bulb have level foot strikes and otherwise balanced feet. Toe and heel length should be assessed, and the hoof-pastern axis should be determined. The angle of the hoof and pastern should be equal to allow equal loading of all portions of the foot. Forelimb hoof-pastern angles normally range from 48 to 55 degrees, but the absolute angle should not be overemphasized. A straight (parallel) pastern-foot axis is more important. A long-toe, underrun-heel foot conformation causes a broken foot axis and predisposes to palmar foot pain (Figure 6-4). The conformation, condition, and integrity of the hoof capsule should be assessed. It is easy to miss hoof wall defects on the medial aspect. Small quarter or heel cracks and defects at the coronary band should not be overlooked. The clinician should evaluate the solar surface, bars, and frog. Thrush, although a reflection of poor management, rarely causes lameness. The shoe type, shoe wear patterns, and the shoe size relative to the foot need to be assessed. The clinician should note the presence of pads or additions to the shoe, such as toe grabs, borium, and heel caulks. There is an association between toe grabs and suspensory apparatus failure in TB racehorses.3 Low heel angle also has been associated with injury.4 Shoe wear is important, because it reflects how the horse has been moving over the last several weeks. The clinician should note the breakover point and whether one branch of the shoe is worn more than the other. Shoe size should be assessed relative to foot size and the fit of the

Fig. 6-2  •  The coronary band is uneven compared with the ground in this trotter’s unbalanced left forelimb hoof. The medial wall (right) appears to be shorter than the lateral wall. A toe weight and bariun point are also shown.

shoe. A shoe that is too small or set too close to the frog may predispose to lameness. Careful palpation of the coronary band in the standing and non–weight-bearing position is critical in detecting foot soreness (Figure 6-5). In horses with sore feet, heat and pain often are detected on the sore side of the foot, and a prominent digital pulse usually is present. Effusion of the distal interphalangeal joint capsule accompanies many abnormalities of the foot, from early synovitis to chronic osteoarthritis of the distal interphalangeal joint, and those with non-specific foot soreness. The clinician places one finger lateral to, and another medial to, the common digital extensor tendon and gently pushes in on the joint capsule, first laterally and then medially. Ballottement is a useful technique to detect effusion in many synovial structures: with effusion, pushing in on the capsule on one side of the tendon causes elevation of the capsule on the other side. The region of the collateral ligaments of the distal interphalangeal joint should be assessed carefully; focal heat or mild swelling may signify acute injury. The clinician should palpate the cartilages of the foot, either with the horse standing or with the limb elevated. Sidebone, mineralization of the cartilages of the foot, rarely causes lameness. The cartilages of the foot normally are pliable and readily compressed axially. Fracture at the

46

PART I  Diagnosis of Lameness

Fig. 6-5  •  Palpation of the coronary band should include assessing the dorsal joint pouch of the distal interphalangeal joint. In this horse, distal interphalangeal effusion and fibrosis appear as a bulge just proximal to the coronary band, dorsally. Fig. 6-3  •  Elevated foot viewed from the palmar aspects shows that the hairline at the medial bulb of heel (on the right) is displaced proximally compared with the lateral heel bulb. The medial wall is longer. Note also the prominent cleft between the heel bulbs. These features are typical of a sheared heel.

Fig. 6-6  •  A variety of hoof testers are available for lameness examinations. I prefer hoof testers that are easily adjusted and used in one hand (two pairs on the right). Large hoof testers (left) can be applied only with two hands, and small hoof testers (bottom) are inappropriate for medium to large hooves.

attachment of the cartilage of the foot to the distal phalanx is an occasional cause of lameness, and compression of the heel with hoof testers may elicit pain in some horses. Horses with sidebone often have medial-to-lateral hoof imbalance.

Hoof Tester Examination Fig. 6-4  •  This trotter has long toe, underrun heel hoof conformation, and broken hoof-pastern axis.

“… I feel naked going into a stall without my hoof testers!”5 Hoof testers are essential for evaluation of the foot and are a basic requirement for all lameness examinations. Many types of hoof testers are available (Figure 6-6), but I favor



Chapter 6  Palpation

47

Fig. 6-7  •  Hoof testers should be applied from the sole to the wall, from heel to toe, and to both sides of the hoof.

one that is adjustable and can be applied with one hand. A proper evaluation of the foot with hoof testers cannot be done with a pad in place, although useful information can be acquired. The instrument can be applied with or without a shoe in place. The amount of force to apply varies from horse to horse and by region of the hoof, and both false-positive and false-negative responses occur. More force is required when the instrument is used across the heel than when used from sole to quarter. The foot should be held between the clinician’s legs in a relaxed manner. The clinician must be able to feel the horse react to subtle pressure, and if the limb is held too tightly or the horse is not calm during the examination, it is difficult to feel a response. The veterinarian should be careful not to place the outside jaw of the instrument too close to the coronary band, because this may cause a false-positive result. Sole sensitivity is assessed by applying the instrument to three to five sites from heel to toe, on both the medial and lateral aspects of the foot, starting from the angle of the sole (seat of the corn) and proceeding dorsally (Figure 6-7). The responses should be compared. If the sole is readily compressible, pain from bruising, a subsolar abscess, laminitis, fracture of the distal phalanx, and other injuries may be elicited, but in horses with hard horn the response may be negative. To evaluate sensitivity of the frog and underlying deeper structures, the hoof testers should be applied from the lateral aspect of the frog to the medial wall, and from the medial aspect of the frog to the lateral wall, each in the palmar, midportion, and dorsal aspects of the frog (Figure 6-8). Pain over the middle third of the frog has been attributed to navicular disease or navicular syndrome, but the specificity of this association is questionable and there are many false-negative responses. Horses with generalized foot soreness or any other cause of palmar foot pain may respond positively or not at all. Only 19 of 42 horses with navicular region pain responded positively to hoof tester examination in the middle third of the frog, with 50% specificity, 50% positive predictive value, and 48% accuracy.6 Horses with palmar foot pain caused by other conditions were as likely to respond to the test, a finding that obviously prompts questioning of the value of hoof tester

Fig. 6-8  •  Hoof testers applied from the middle of the frog to the contralateral hoof wall put pressure on the navicular region. Horses with many abnormal conditions of the hoof may manifest a positive response.

examination.6 It is difficult if not impossible to create adequate pressure to cause pain in large breed horses or if the horn is hard. Application of a poultice or soaking the foot may be necessary to soften a hard foot, and reexamination after several days may be rewarding. Hoof tester application to the small feet of foals or ponies may elicit a false-positive response, and hoof tester size or amount of compression may require adjustment. Application of hoof testers across the heel may cause pain in horses with palmar foot pain but is not specific (Figure 6-9). Application of the hoof tester to the area of the sole adjacent to each nail, nail hole, or defect in the sole or white line is useful to detect a subsolar abscess or a close nail (Figure 6-10). Areas of pain can be gently explored with a hoof knife, but unless clearly indicated, the veterinarian should refrain from digging too deeply. The hoof tester can then be used as a hammer to percuss each nail in the shoe and the frog and toe regions. After completing the hoof tester examination, the clinician should reassess the digital pulses. In horses with foot pain the digital pulse may now be bounding. Horses that have recently been shod or trimmed or have raced or performed recently, especially on hard surfaces, may have mild elevations in digital pulse amplitude and may show hoof tester sensitivity normally. Pain causing lameness may not be in the foot.

Wedge Test and Other Forms of Static Manipulation

The wedge test is used most commonly as a dynamic procedure to induce lameness during the movement phase of the examination, but can be used to assess the static response of a horse to dramatic changes in dorsal-topalmar or medial-to-lateral hoof angles (see Chapter 8, Figure 8-12). A digital extension device, with which the author gauged static painful responses to changes in hoof

48

PART I  Diagnosis of Lameness

Fig. 6-11  •  Palpation of oblique distal sesamoidean ligaments.

angle to make shoeing recommendations, was recently described.7

present for fluid distention to be perceived. Bony swelling associated with this joint, proximal or high ringbone, is a classic cause of lameness yet an unusual clinical finding. Osteoarthritis of the proximal interphalangeal joint is a common diagnosis, but one made by a combination of clinical findings, diagnostic analgesia, radiography, and sometimes scintigraphy. The distal extent of the digital flexor tendon sheath (DFTS), deep digital flexor tendon (DDFT), and distal sesamoidean ligaments are palpated. Deep pain associated with the origin and insertion of the distal sesamoidean ligaments is assessed by palpation with the limb in flexion (Figure 6-11). In some horses with lesions of the DDFT within the hoof capsule a positive response to compression of the palmar pastern region is present, but this finding is inconsistent and many false-negative responses occur. The oblique sesamoidean ligaments are difficult to differentiate from the branches of the SDFT, but injury of the SDFT is more common. Distal sesamoidean desmitis or chronic suspensory desmitis may result in subluxation of the proximal interphalangeal joint (Figure 6-12). Swelling should prompt ultrasonographic examination if relevance has been confirmed using diagnostic analgesia. The proximal interphalangeal joint is manipulated in a medial-to-lateral direction to assess pain and collateral ligament integrity and is flexed independently of the fetlock joint. The proximal, dorsal aspect of the proximal phalanx is palpated (Figure 6-13). Horses with short, midsagittal fractures or dorsal frontal fractures of the proximal phalanx or proliferation at the attachment of the common digital extensor tendon may show pain. Enthesophyte formation at the common digital extensor tendon attachment, seen most commonly in older ex-racehorses with chronic osteoarthritis of the fetlock joint, results in prominent bony and soft tissue swelling and pain on palpation.

Pastern

Fetlock

Fig. 6-9  •  Adjustable hoof testers are easily placed across the heel. I prefer to apply hoof testers in this manner to assess horses for palmar foot pain during static examination and as a provocative test for lameness.

Fig. 6-10  •  Acute, severe lameness causing increase in digital pulse and profound hoof tester sensitivity in the toe region resulted from this hoof abscess. Exudate drains from the pared region at the toe. (Courtesy Greg Staller, Pottersville, New Jersey.)

The proximal interphalangeal (pastern) joint capsule is assessed by ballottement, although severe effusion must be

The clinician palpates the joint capsule of the metacarpophalangeal (fetlock) joint with the limb bearing weight,



Chapter 6  Palpation

49

Fig. 6-14  •  Digital pulse quality can be assessed easily at the level of the proximal sesamoid bones.

Fig. 6-12  •  Subluxation and osteoarthritis of the left front proximal interphalangeal joint resulted from primary suspensory desmitis.

Fig. 6-13  •  Proliferative changes at the common digital extensor attachment or pain from midsagittal fracture of the proximal phalanx should be palpated along the dorsal, proximal aspect of the proximal phalanx.

keeping in mind that pain associated with the joint can be present without localizing clinical signs. The dorsal aspect is palpated using ballottement on either side of the common digital extensor tendon. The clinician should determine whether localized heat is present. Osselets is a North American term used to describe early osteoarthritis of the metacarpophalangeal joint in young racehorses, with firm bony

and soft tissue swelling on the dorsal, medial aspect of the proximal phalanx, and the distal aspect of the McIII, caused by traumatic capsulitis and early enthesophyte formation. Occasionally in horses with prominent effusion of the metacarpophalangeal joint, a soft tissue swelling can be palpated in the proximal, dorsal aspect of the joint from excessive proliferation of the dorsal synovial pads, called proliferative or villonodular synovitis. The palmar pouch of the metacarpophalangeal joint is palpated dorsal to the SL branches, both medially and laterally. Mild effusion may be present without associated lameness, especially in older performance horses. The PSBs are palpated and assessed for mild swelling and heat, clinical signs of sesamoiditis, or SL avulsion injury. The digital pulse amplitude is reassessed by placing fingers both medially and laterally, abaxial to both PSBs (Figure 6-14). The DFTS extends from the distal metacarpal region to the distal palmar aspect of the pastern. Usually no palpable fluid is found. Effusion of the DFTS (tenosynovitis) causes swelling in the palmar fetlock region that must be differentiated from effusion of the metacarpophalangeal joint. Tenosynovitis causes swelling palmar to the branches of the SL, medially and laterally. Fluid can be compressed from medial to lateral. With severe effusion, distention is found in the palmar aspect of the pastern, but there may be distention proximal to the palmar annular ligament without obvious distention distally. Wind puffs or windgalls describe incidental fluid distention of the DFTS, commonly seen in older performance horses unassociated with lameness. Tenosynovitis can cause lameness, but additional diagnostic techniques are required to confirm the diagnosis. The limb is elevated to assess range of joint motion and the horse’s response to flexion. Normally the fetlock can be flexed to 90 degrees (the angle between the proximal phalanx and the McIII) or slightly more. A reduction in fetlock flexion range is indicative of chronic fibrosis but is

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PART I  Diagnosis of Lameness

not necessarily a cause for concern. A pronounced response to static flexion is noteworthy, although many horses resent static flexion but do not show a positive response to dynamic flexion (lower limb or fetlock flexion tests; see Chapter 8). Horses with clinically relevant tenosynovitis usually strongly resent fetlock flexion. With the limb in flexion, the clinician palpates the PSBs and the branches of the SL, avoiding compression of the palmar digital nerves.

Metacarpal Region

The clinician should assess the dorsal aspect of the McIII for heat and swelling. This is a common area for traumatic injury (barked shins) or stress-related bone injury (bucked shin syndrome). Many ex-racehorses have incidental, prominent, chronic, and nonpainful swelling of the McIII caused by extensive modeling and remodeling of the dorsal cortex while in race training. Racehorses currently in training may have heat and pain on deep palpation (performed with the limb elevated), but prominent swelling may be lacking. Any combination of palpation findings is possible in horses with stress-related bone injury of the McIII. It is difficult to apply deep pressure to the dorsal aspect of the McIII without concomitant pressure to the palmar soft tissue structures or PSBs, so the responses should be assessed carefully. The entire length (abaxial surface) of the second and fourth metacarpal bones (McII/IV) should be palpated with the horse in the standing position to detect exostoses, callus, or fractures. Swelling of the SL branches or body may make this difficult. Palpation of the McII and the McIV should be repeated with the limb elevated, because the axial aspect of these bones is impossible to assess in the weight-bearing position. Splint exostoses are common, particularly in young horses. Therefore the presence of even large bony swellings is not unusual. Exostoses detected axially, possibly impinging on the SL or causing adhesions to the SL (or so-called “blind splints”) should be carefully noted. Both false-positive and false-negative results can occur when palpating a splint exostosis and results of palpation and compression should be confirmed using perineural analgesia. Pain from even small exostoses of the McII and the McIV usually is more accurately assessed immediately after training or racing, because pain and lameness resulting from these swellings can be subtle and transient. The clinician should carefully palpate the SL branches. Differentiation of branch or SL body injuries is important: the latter injuries usually are more serious and have a worse prognosis. The medial and lateral palmar digital vein, artery, and nerve, in dorsal-to-palmar orientation, respectively, are located between the SL and DDFT. The accessory ligament (distal or inferior check ligament) of the DDFT (ALDDFT) normally is difficult to palpate and even when enlarged cannot easily be differentiated from the DDFT, but injuries of the ALDDFT are more common. All soft tissue structures should be palpated carefully, using digital compression, with the limb elevated (Figure 6-15). Acute or chronic swelling should be assessed, as should the horse’s response to deep palpation. Obvious swelling and pain indicate the presence of tendonitis or desmitis. In some horses with acute severe tendonitis or desmitis the structure feels “mushy” or soft in the area of fiber damage. This finding, especially in horses with fetlock drop, indicates near rupture of the structure. There are many false-positive and

Fig. 6-15  •  The soft tissue structures in the palmar metacarpal region should be carefully palpated with the horse in standing and flexed (shown) positions for heat, pain on compression, and swelling. Most ridden horses have mild pain, but in racehorses a painful response is an early sign of tendonitis or desmitis.

even false-negative responses to palpation of the digital flexor tendons and SL. In most ridden performance horses a mild painful response (false-positive) to deep palpation of the SL is normal. However, in racehorses, false-positive responses are less common, and a painful response to deep palpation may indicate the presence of early desmitis or tendonitis. In many horses with foot lameness, secondary, mild suspensory desmitis is common. There is a painful response to palpation of the body and origin of the SL. It may be difficult to decide whether this is a true or falsepositive response, a determination that often is made in hindsight after the lameness examination is finished. Falsepositive and false-negative responses to palpation of the proximal palmar metacarpal region also occur. This is a common site of lameness and should be examined carefully. Palpation must be done with the limb in flexion, and the presence of swelling and pain must be carefully interpreted (Figure 6-16). Horses with acute injuries, such as proximal suspensory desmitis (PSD), avulsion or longitudinal fracture of the McIII, and stress reaction of the McIII at the origin of the SL, may have swelling and pain. Deep palpation may create pressure on the palmar metacarpal nerves resulting in a false-positive pain response, and many horses with PSD have no localizing signs. The most proximal aspect of the SDFT is difficult to palpate with the limb in a flexed position, and mild swelling from tendonitis can easily be missed. When the limb is weight bearing, the expected convex profile associated with SDF tendonitis in the mid-to-distal regions of the metacarpal region is usually not seen because of pressure from the overlying metacarpal fascia. Careful palpation of the proximal aspect of the SDFT, particularly in horses that negotiate fences or in ponies, is necessary to avoid missing subtle lesions. This injury is particularly hard to recognize in horses or ponies with long hair coats. The proximal dorsal aspect of the McIII should be palpated in a flexed position (Figure 6-17). Occasionally, dorsomedial articular fracture of the McIII results in a subtle

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Fig. 6-16  •  Palpation of the proximopalmar metacarpal region is essential in diagnosing proximal suspensory desmitis and other conditions of the suspensory origin and differentiating lameness in the region from carpal lameness. (Courtesy Ross Rich, Cave Creek, Arizona.)

Fig. 6-18  •  Carpal tenosynovitis must be differentiated from effusion of the antebrachiocarpal joint. This horse with severe superficial digital flexor tendonitis has moderate distention of the carpal sheath (arrow) in the caudal, distal aspect of the antebrachium and medially in the proximal metacarpal region (not shown).

Carpus

Fig. 6-17  •  Careful palpation of the proximal, dorsal metacarpal region identifies pain associated with dorsomedial articular fracture or other fractures of the proximal aspect of the third metacarpal bone. (Courtesy Ross Rich, Cave Creek, Arizona.)

painful swelling. Swelling (effusion) of the carpal sheath may be detected in the proximal medial metacarpal region, but large veins (medial palmar, accessory cephalic, and cephalic veins) may interfere with accurate palpation. With mild tenosynovitis, effusion may be difficult to discern.

Detection of warmth on the dorsal aspect of the carpus is a reliable indicator of underlying inflammation. Obviously, one side should be compared with the other, but bilateral conditions exist commonly. Previous application of counterirritants interferes with the reliable detection of warmth. Carpal joint lameness without obvious signs of synovitis is common, but if present, effusion is easily palpated using ballottement. With the horse in the standing position, a finger is placed dorsolaterally between the extensor carpi radialis and common digital extensor tendons, and another finger is placed just medial to the extensor carpi radialis tendon. These openings are used for palpation and arthrocentesis of both the middle carpal and the antebrachiocarpal joints. The middle carpal and the carpometacarpal joints always communicate, but a small synovial compartment and dense overlying soft tissue structures limit palpation of the carpometacarpal joint. Both the middle carpal and the antebrachiocarpal joints have a palmarolateral pouch that may be distended if effusion is severe. If swelling is detected just caudal to the radius, it is necessary to differentiate distention of the palmarolateral pouch of the antebrachiocarpal joint from the carpal sheath (Figure 6-18). In horses with antebrachiocarpal joint effusion the dorsal outpouchings also should be prominent, whereas in those with carpal sheath effusion, fluid distention is restricted to the palmar aspect and also detected medially, both proximal and distal to the accessory carpal bone.

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PART I  Diagnosis of Lameness

Tenosynovitis of the extensor carpi radialis, common digital extensor, or lateral digital extensor sheaths results in vertically oriented swellings that traverse the carpal joints, may extend proximal or distal to the carpus, and usually are multilobed, being divided by bands of extensor retinaculum located dorsally and laterally. Normally the carpus can easily be flexed completely, so that the palmar metacarpal region and bulbs of the heel touch the caudal aspect of the antebrachium. Reduced flexion may be caused by pain, with or without chronic fibrosis, associated with osteoarthritis. Pain during carpal flexion is a reliable indicator of carpal region pain but does not indicate the cause. The carpal sheath is compressed and the extensor tendons are stretched during this maneuver, and conditions involving these structures and the accessory carpal bone can cause pain during flexion. The elbow joint is flexed simultaneously; therefore a positive response to carpal flexion can rarely result from elbow pain. The examiner should palpate the dorsal surfaces of the carpal bones with the limb in partial flexion (Figure 6-19). Many pathological conditions associated with the carpus are manifested dorsally, and pain associated with osteochondral fragmentation, slab fractures or other severe injuries, or osteoarthritis can be assessed with the limb in this position. Focal pain can be identified, and loose fragments associated with the third carpal bone or distal lateral radius occasionally can be identified.

A

Antebrachium (Forearm)

Digital palpation of the forearm usually is performed with the limb bearing weight. The examiner should look primarily for muscle atrophy, wounds, or mild swelling associated with the radius. Small wounds in the antebrachium may look innocuous, but inappropriately severe lameness and pain on palpation may reflect a spiral radial fracture. The examiner should pay particular attention to the medial aspect of the limb; this area is easily overlooked when palpating from the lateral side. Distally, fluid distention of the carpal sheath or acute swelling associated with injury of the accessory ligament (proximal or superior check ligament) of the SDFT, or the flexor muscles and tendons can occur. The amount of muscle in the extensors and flexors should be compared with that in the contralateral limb, because subtle atrophy may be missed during observation.

Elbow

Frank swelling and prominent lameness accompany many injuries of the elbow region, but other problems of the elbow joint are discovered only after diagnostic analgesia has localized pain to this area or by use of advanced imaging modalities. It is nearly impossible to use diagnostic analgesic techniques to abolish pain in the distal aspect of the humerus and proximal aspects of the radius and ulna; therefore advanced imaging techniques are often required to identify problems in these structures. The clinician should palpate the olecranon process and the lateral and medial collateral ligaments with the limb bearing weight. Effusion is difficult to detect, but excess fluid occasionally can be found using ballottement, by placing fingers both cranial and caudal to the lateral collateral ligament. The elbow is flexed by pulling the distal limb in a cranial and proximal direction and then extended by

B Fig. 6-19  •  Careful palpation of the dorsal aspect of each carpal bone can be done with one hand (A) or by placing the distal limb between the clinician’s legs and using both hands (B). A pain response indicates an osteochondral fragment or an osteophyte. Occasionally a loose osteochondral fragment can be palpated.

pulling the lower limb in a caudal direction. The shoulder joint is undergoing the opposite reaction during this manipulation, and pain associated with that joint or the bicipital bursa can cause a positive response during elbow manipulation.



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Chapter 6  Palpation

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Brachium (Arm) and Shoulder

The shoulder and intertubercular (bicipital) bursa are regularly blamed as the cause of lameness yet are seldom involved. Normal horses may resent palpation of this area. Pain in the muscles surrounding the shoulder joint may develop secondary to primary lower limb lameness. In Standardbred (STB) racehorses with carpal lameness, secondary pain often is detected when the bicipital bursa is palpated. A rare cause of lameness is infection as a result of a previous deep injection of the “shoulder bursae,” and horses may have only subtle pain on palpation and manipulation of the shoulder region. Infectious bicipital bursitis generally causes severe lameness, a marked shortened cranial phase of the stride, and a marked painful response to shoulder joint flexion. Palpation of the arm is limited because overlying muscles obscure much of the humerus. Horses with displaced humeral fractures usually are unwilling to bear weight and have severe soft tissue swelling. Those with humeral stress fractures usually have no localizing signs except a positive response to upper limb manipulation. A normal intertubercular bursa is not palpable. Horses with bicipital bursitis usually resent direct compression of the greater tubercle of the humerus, and fluid distention may be palpable, but ballottement is usually limited. Effusion of the scapulohumeral (shoulder) joint is palpable only if severe and even then is easily overlooked. Upper limb manipulation, including static flexion and extension to assess the range of motion of the shoulder and elbow joints and the presence of a painful response, should always be performed. This can be done during palpation of the elbow or later when the clinician finishes the shoulder region. Most horses with shoulder joint lameness or bicipital bursitis show a painful response when the limb is pulled backward (shoulder flexion, elbow extension), whereas those with elbow lameness may show a painful response when the limb is pulled forward (shoulder extension, elbow flexion). The examiner should palpate the scapular area and move the mane if necessary. Atrophy of the infraspinatus and supraspinatus muscles may indicate suprascapular nerve or brachial plexus injury (Figure 6-20). Muscle atrophy of these and other forelimb muscles can be caused by other neurogenic causes or by disuse. Upper limb palpation often is used to confirm those findings recognized during observation of the horse. Scapular height is compared manually. Although rare, damage to the innervation of the serratus ventralis muscle or direct trauma to the muscle itself allows abnormal elevation of the injured side when the horse is standing or during movement. Pectoral muscle atrophy can easily be missed during observation, and the pectoral region should be palpated to assess pectoral muscle mass and identify swellings or wounds that may cause lameness.

PALPATION OF THE CERVICAL AND THORACOLUMBAR SPINE Cervical Spine (Neck)

Palpation of the neck is limited. I usually palpate the brachiocephalicus muscle after shoulder palpation and manipulation, a procedure thought to have predictive but

Fig. 6-20  •  This horse shows atrophy of the supraspinatus and infraspinatus muscles with concomitant lateral subluxation of the left shoulder joint.

nonspecific value in horses with forelimb lameness.8 The muscle is squeezed just cranial to the shoulder joint; most horses flinch, but some horses with ipsilateral forelimb lameness show a marked pain response. The examiner should palpate both sides of the neck, noting any swelling or muscle atrophy. Cervical abscessation can cause signs of neck pain and forelimb lameness. Muscle atrophy may indicate long-standing cervical pain or ipsilateral forelimb lameness. Muscle development of the neck may be asymmetrical, especially if viewed from above (the perspective of a rider).2 Palpation of the poll region is important because undue soreness cranial to the wings of the atlas may be associated with poor performance.2 The head should be moved from side to side to evaluate the horse’s willingness to move the neck. One hand is placed on the midcervical region to use as a fulcrum, and the other hand is used to bend the head and neck toward the examiner. Food also can be used to entice the horse to move the head and neck from side to side. Normally a horse can reach around to the girth region on either side to ingest food, and reluctance to do so may indicate neck pain. This procedure may more closely mimic the horse’s natural head and neck movement than using a hand in the midcervical area as a fulcrum. A more comprehensive examination, including neurological or chiropractic evaluations, may be necessary after completion of the lameness examination.

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PART I  Diagnosis of Lameness

Up-and-down movement of the head also should be assessed. Although usually not a part of a routine lameness examination, evaluation of the temporomandibular joints and the mouth may be necessary in horses with poor performance.2

Thoracolumbar Spine (Back)

Additional detailed palpation of the back and pelvis may be necessary once the lameness examination has been completed. Chiropractic manipulation and assessment of acupuncture points may be useful but usually are reserved for specific horses or when history and clinical signs warrant such an examination and if the clinician is qualified to complete it. The cranial thoracic spine has already been briefly evaluated during examination of the shoulder for scapular symmetry. The withers should be examined closely for conformational abnormalities, such as those seen with fracture of the dorsal spinous processes or fistulous withers. The presence of sores may indicate an ill-fitting saddle and can cause performance-related problems. Using a hand on each side of the spine, the examiner should apply digital pressure to assess vertebral height, presence of pain, and muscle atrophy and to confirm symmetry (Figure 6-21). Many horses resent deep and aggressive palpation of the epaxial muscles, and the response of normal horses should be learned before a pathological response is presumed. Most horses readily become mildly lordotic (“scootch”) during deep digital palpation or when a blunt object, such as a pen, is used. Some clinicians prefer to use the ends of the fingers to “run” (apply digital pressure while moving the fingers caudally) the muscles from cranial to caudal, parallel to the spinal column. When this is continued along the gluteal muscles and rump, most normal horses become somewhat kyphotic and move forward slightly. Aggressive use of blunt or sharp objects to assess pain should be avoided. Some horses are stoic during palpation, and it may be impossible to stimulate them to extend and flex the thoracolumbar region without the use of a blunt instrument.2 In these horses, firmly stroking the ventral abdomen may stimulate movement.2 With one hand on the horse’s back during movement of the

thoracolumbar spine, the clinician may be able to feel muscle “cracking” during the release of tension in the epaxial muscles.2 The observation of muscle fasciculations during or after palpation usually indicates a degree of muscle pain. Failure to exhibit the normal lordotic or kyphotic responses, assumption of a guarded posture, and vocalization during the examination are further signs of back pain. In many horses, back pain, and more specifically muscle pain, is secondary to hindlimb lameness, resulting from altered gait and posture. Any site of pain in the hindlimb may alter the gait to cause secondary upper limb or back muscle pain. The use of diagnostic analgesia to confirm the primary source of pain (in the hindlimb, or locally in the back) may be required to make the true diagnosis. Back pain often is complex and may be caused by many factors including ill-fitting saddles, poor riding, and other primary problems, such as overriding of dorsal spinous processes or other bony causes. The clinician should palpate carefully to detect localized swelling in the area of the saddle. Even small areas of hair loss without swelling may indicate a loose or ill-fitting saddle, abnormal movement of the saddle associated with hindlimb lameness, or a rider sitting crookedly.2 It is doubtful that muscular pain alone can cause unilateral hindlimb lameness. Back pain was induced in STB horses by injection of lactic acid into the left longissimus dorsi muscle and subsequently exercised and observed with high-speed cinematography.9 Frank lameness was not observed, but there was slight modification of left hindlimb stride and reduced performance. This supports the clinical observation that back pain usually is the result, not the cause, of obvious hindlimb lameness, although it may result in slight alterations in gait. Severe vertebral abnormalities or an abscess in the epaxial muscles may result in lameness or neurological dysfunction.

PALPATION OF THE LATERAL AND VENTRAL THORAX AND ABDOMEN History or observation of lameness, performance, or behavioral abnormalities seen only when a horse is ridden or wearing tack should prompt examination of the thoracic region. Irritation from an ill-fitting girth or other sores or wounds can contribute to poor performance, and injury of the sternum or ribs can cause pain associated with saddling or being ridden. Traumatically induced hernias of the ventral abdomen can cause gait deficits or guarding of the abdomen.

PALPATION OF THE EXTERNAL GENITALIA Testicular or inguinal pain should be considered as a cause of gait modification. Swelling, infection from previous castration, scirrhous cord, and mastitis can cause a change in gait. The veterinarian should determine the sex of the horse and the presence of one or both testicles.

Fig. 6-21  •  Palpation of the thoracolumbar region should be performed in a quiet, careful manner. Many horses object to sudden or sharp stimuli applied to this region. Direct, even pressure is applied to the epaxial muscles (shown) and the summits of the dorsal spinous processes.

PALPATION OF THE PELVIS Palpation of the pelvis is performed to confirm previous observations. The horse should stand as squarely as possible. The clinician should palpate all bony protuberances,



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Fig. 6-23  •  The tubera ischii (shown) and third trochanters are palpated carefully. Enthesopathy or fracture causes lameness that is difficult to locate without careful palpation or scintigraphic examination. Occasionally, horses with small muscle defects located distal to the tubera ischii have chronic lameness from previous fracture. (Courtesy Carolyn Arnold, College Station, TX.)

Fig. 6-22  •  Although the veterinarian must take care when standing behind any horse, this perspective is crucial in determining pelvic heights and widths. The height of each tuber coxae is compared in this photograph. Alternatively, an assistant on each side can be asked to point to a comparable location, or tape can be applied.

Muscle pain and muscle atrophy should be assessed. The clinician carefully examines the gluteal musculature, the origin of the caudal thigh muscles, and the tensor fasciae latae (see Chapter 47 for further discussion of muscle assessment and palpation of the greater trochanter of the femur). Pain or soreness noted during palpation of the semimembranosus and semitendinosus muscles may be associated with injury of the ipsilateral tuber ischium.2

PALPATION OF THE PELVIS PER RECTUM including the tubera coxae, tubera sacrale, and tubera ischii. The examiner stands behind the horse and palpates these paired protuberances simultaneously if it is safe to do so (Figure 6-22). Fracture of a tuber coxae or an ilial shaft may result in asymmetry, but if the ventral aspect of the tuber coxae is fractured, the height of the dorsal aspect may be equal to that of the contralateral side. The anatomy of the ventral aspect of the tuber coxae is distorted. Small muscle defects may be associated with fracture or enthesopathy of the tubera ischii, but even with a displaced fracture, palpation of this area may be unrewarding (Figure 6-23). If a pelvic injury or fracture is suspected, the clinician should gently rock (move) the horse from side to side. Subtle crepitus may be detected, but in many horses with pelvic fractures this is not apparent until days to weeks after injury and only during the initial portions of the examination before muscle guarding supervenes. The veterinarian should grasp the tail and elevate it. Many horses resist this, but in those with fractures of the base of the tail (most commonly from sitting in the starting gate or trailer), a true pain response is elicited. Subtle swelling also may be present. Lack of tail tone may indicate neurological disease.

Rectal examination is not part of the routine lameness examination and should be reserved as a special examination procedure if pelvic fracture or aortoiliac thrombosis is suspected. With the wrist just inside the anus the veterinarian should palpate the medial and dorsal aspects of the acetabulum, comparing sides. In young horses, there is a membranous junction between pelvic bones in the center of the acetabulum; a defect and a small amount of motion normally can be felt. Just cranial to the acetabulum is the cranial aspect of the pubis (brim of the pelvis). With the arm at elbow depth the examiner should sweep the arm dorsally on each side to palpate the medial aspect of each ilium. The ventral aspect of the sacrum and sacroiliac region are compared. The clinician should compare the pulse quality between the right and left external iliac arteries and evaluate conformation and pulse quality of the terminal aorta and branches. Horses with aortoiliac thromboembolism have abnormal conformation and altered pulse quality. Crepitus may be felt more easily by gently rocking the horse from side to side, picking up one hindlimb, or walking the horse a short distance with the veterinarian’s arm still within the rectum. Asymmetry, swelling, actual fracture lines, fragments or callus, and crepitus are assessed. In horses with acute pelvic

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PART I  Diagnosis of Lameness

fractures, crepitus, fracture fragments or lines, and callus usually are not detectable, but hematoma and soft tissue swelling usually can be felt. In horses with ilial wing or shaft fractures, large fracture hematomas often are present, but the absence of swelling does not preclude presence of ilial fractures. These horses are at risk to develop fatal hemorrhage. Edges of fracture fragments may be evident with comminuted or grossly displaced fractures. With chronic pelvic fractures, crepitus and callus may be more obvious.

PALPATION OF THE HINDLIMB For safety reasons, I prefer to start proximally and work distally in a hindlimb, allowing the horse to become accustomed to palpation. Horses often object to palpation of the flank and stifle regions, and this should not be misinterpreted as a sign of pain. The clinician should grasp the tail and pull it gently toward himself or herself to keep the ipsilateral hindlimb bearing weight and reduce the chance of the horse kicking. It may be useful to pick up the ipsilateral forelimb. In the large majority of horses the entire limb can be safely examined while bearing weight, but pain in the lame limb or contralateral limb or the horse’s behavior may make it difficult or impossible to pick up the limb. Reluctance to pick up the hindlimbs has been attributed to unilateral or bilateral sacroiliac pain.2 Horses with shivers often are reluctant or anxious to pick up one or both hindlimbs. It may be necessary to spend a small amount of time coaxing the horse to elevate the hindlimb, at first just high enough to examine or pick out the hind foot and then progressing to full flexion. Although historically the hock and stifle joints have been regarded as the principal sources of pain causing hindlimb lameness, there are many other potential sites, and the metatarsal and fetlock regions in particular should be examined with care.

Thigh

The clinician should assess the thigh for swelling, muscle atrophy, or scarring. Horses with femoral fractures usually have obvious severe swelling, crepitus, and instability of the limb. The third trochanter of the femur is difficult to feel, and clinical abnormalities associated with enthesopathy of the insertion of the superficial gluteal muscle or a fracture usually are impossible to detect. Scarring associated with the semitendinosus, the semimembranosus, and rarely the biceps femoris can lead to mechanical gait deficits, known as fibrotic myopathy. The gastrocnemius muscle arises from the distal caudal aspect of the femur, and acute tearing of this muscle may cause swelling in the caudal stifle area. This is difficult to perceive, but severe muscle injury results in a marked postural change, which should provoke more careful assessment of this region.

Stifle

Palpation of the stifle is limited to the cranial, lateral, and medial aspects; unfortunately, the caudal and proximal aspects of the joint are inaccessible. Many horses, especially fillies, object to palpation of the stifle, a normal response often misinterpreted as a painful reaction. The veterinarian should palpate the stifle with the limb bearing weight. The foot should be flat on the ground. This may be impossible if the horse has severe pain prohibiting complete assessment of the stifle. The limb should be in a

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neutral and not in an abducted position and should be perpendicular to the spine or slightly ahead of the other hindlimb. If the limb is retracted, it is more difficult to palpate the patellar ligaments and joint outpouchings. The middle patellar ligament is identified and followed proximally to the distal aspect of the patella. The clinician should feel the femoropatellar joint capsule between either the middle and medial or the middle and lateral patellar ligaments and should determine the presence of effusion. In horses with osteochondritis dissecans (OCD), fluid distention can be pronounced. However, normal young horses (weanlings to early 2-year-olds) often have prominent bilateral fluid distention of the femoropatellar joint capsules. The clinician should find the medial patellar ligament and follow it proximally and distally. At the proximal extent, the medial fibrocartilage of the patella can be felt medial to the medial trochlear ridge of the femur. It is this normal arrangement of the medial aspect of the patella and the medial trochlear ridge that allows the veterinarian to determine whether a horse has patellar luxation. The position of the patella is difficult to confirm if the horse is standing with the stifle flexed. True patellar luxation is rare. The examiner should determine if the medial patellar ligament is enlarged, which usually reflects previous desmotomy or dermoplasty. Usually a distinct depression is present between the medial patellar ligament and the medial collateral ligament, but effusion of the medial femorotibial (MFT) joint may result in a substantial “bulge” (Figure 6-24). This may be the only clinical sign indicative of MFT joint injury. The lateral and middle patellar ligaments are palpated from their origin to insertion. Patellar desmitis is unusual but does occur; it usually involves the middle patellar ligament and may cause mild swelling. Previous injection with counterirritants causes firm, fibrous areas over the patellar ligaments, a common finding in racehorses. Gently rocking the horse from side to side to assess motion of the patella may give some indication of the potential for intermittent upward fixation of the patella (IUFP). In horses prone to IUFP, jerky rather than the normal smooth motion of the patella sometimes is detected.2 The lateral femorotibial (LFT) joint capsule is accessed between the lateral patellar and lateral collateral ligaments, but even with severe effusion it may be difficult to palpate. Overlying and adjacent soft tissue structures obscure palpation. Effusion of the LFT joint, although rare, is an important palpation finding that should be investigated carefully. Deep palpation of the medial collateral ligament and the medial patellar ligament with the limb in flexion may elicit a pain response in horses with stifle lameness, but it probably is not specific for the source of pain in the stifle. The medial collateral stress test is perhaps the most reliable manipulative test of the stifle, although horses with lower limb lameness also may respond. With the leg in partial flexion, the shoulder or one hand is used as a fulcrum on the lateral aspect of the stifle, and the distal extremity is pulled laterally, thus placing valgus stress on the stifle (Figure 6-25). Care should be taken because horses may resent this manipulative test. If possible, the valgus motion should be applied by using the shoulder as a fulcrum and both hands on the crus, thus eliminating possible falsepositive results from the lower limb. Patellar manipulation may cause a pain response, particularly in horses with

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Fig. 6-26  •  Used as a static or provocative test, patellar manipulation is performed by placing the palm of the hand over the cranial aspect of the patella and manually forcing the patella proximally several times in succession. This maneuver can exacerbate pain from conditions of the patella and femoropatellar joint and forces the distal femur in a caudal direction. Pain from soft tissue injuries such as patellar, cruciate, or collateral ligament tears and osteoarthritis of the femorotibial joints can be exacerbated, but false-negative and false-positive results are common. (Courtesy Carolyn Arnold, College Station, TX.) Fig. 6-24  •  The medial femorotibial joint (right stifle, cranial view) is the most common location for osteoarthritis of the stifle joint and is palpated medially (needle in joint) between the medial patellar ligament and the medial collateral ligament. Normally a depression is present at this location, but a bulge from effusion can be palpated in this horse.

femorotibial joint disease. During this procedure, caudal movement of the femur also may exacerbate cruciate injuries. With the limb on the ground in a weight-bearing position, the clinician’s hand is placed on the distal aspect of the patella, and the patella is forced upward (Figure 6-26). Theoretically during this test, numerous movements of the stifle are induced. The patellar ligaments are stretched, the patella is forced proximally, and on release the patella rapidly moves distally against the trochlear ridges, and the femur is forced caudally. Tests to assess cruciate ligament damage have been described but are dangerous to perform, and I have not found them particularly useful.10 Complete tearing of the cruciate or collateral ligaments is rare, and partial tearing does not cause clinically detectable instability. In horses with severe lameness and gross stifle instability, it is obvious that the stifle is the source of lameness, and pain usually prohibits manipulation.

Crus

Fig. 6-25  •  The valgus stress test of the stifle is difficult to perform and is accomplished by using a hand (shown) or shoulder as a fulcrum. This test can be done during static examination or a provocative test followed by trotting (see Chapter 8).

The examiner should palpate the crus using both hands with the limb bearing weight. Subtle swelling of the medial aspect of the tibia can be palpated, but palpation of the caudolateral aspect of the tibia, the area in which stress fractures are diagnosed most frequently, is limited. Often no palpable abnormality is associated with a stress fracture. Any small wound or any form of swelling should be thoroughly investigated for the possibility of underlying bone damage, such as an occult tibial fracture. The veterinarian should palpate the caudal soft tissues.

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PART I  Diagnosis of Lameness

A

B

Fig. 6-27  •  A, Palpation of the medial aspect of the tibia in a flexed position or B, tibial percussion in the standing position sometimes elicits pain in horses with tibial stress fractures, but false-positive results are common.

Proximally, the musculotendonous junction of the gastrocnemius muscle is a rare site of pain. The common calcaneal tendon is assessed. Swelling may indicate damage to any one of the contributing tendons. Effusion of the tarsal sheath causes swelling just proximal to the tarsus, at the caudal aspect of the crus, and should be differentiated from bog spavin. Deep palpation of the medial and caudal aspects of the crus is performed with the limb elevated (Figure 6-27). Horses with tibial stress fractures or those with spiral fracture or other tibial trauma may show a pain response, but false-positive responses are frequent. Tibial percussion, performed medially by using a clenched fist (knuckles) as a hammer, may elicit a pain response in horses with stress fractures, but many normal horses resent this test.

Tarsus

Five common swellings of the hock are important to differentiate, but hock swelling is not synonymous with hock pain. Capped hock is swelling located at the point of the hock (the proximal aspect of the calcaneus) and usually is an incidental finding, but in some horses the condition does cause lameness (Figure 6-28). The most common form involves the development of firm, fibrous subcutaneous tissue in the false bursa that lies over the point of the hock. This is a common area for abrasions and excoriation, and fibrous tissue formation results in a blemish but usually no lameness. Horses may be sensitive to palpation if the area has been traumatized recently. Infection or trauma leading to osteitis of the calcaneus can cause a clinically important capped hock and severe lameness. In these horses the problem involves the calcaneal bursa, located between the common calcaneal tendon and the calcaneus. If surrounding soft tissue swelling is minimal, fluid distention of the calcaneal bursa may be felt by

Fig. 6-28  •  Capped hock, a firm fibrous swelling of the proximal aspect of the calcaneus (point of the hock), is considered a blemish, but with effusion of the calcaneal bursa (not shown), lameness is substantial.

ballottement. The bursa can be felt both medially and laterally at the proximal aspect of the calcaneus. Lateral, or less commonly, medial dislocation (luxation) of the SDFT results in similar swelling, but in an acute situation, lameness is present. Careful palpation may reveal the SDFT coursing laterally (Figure 6-29), unless excessive soft tissue swelling is present.



Fig. 6-29  •  Lateral dislocation (luxation) of the superficial digital flexor tendon. Instead of attaching to the tuber calcanei, the superficial digital flexor tendon (arrows) is now located lateral to the point of the hock. Initial swelling makes this diagnosis difficult.

Effusion of the tarsal sheath, thoroughpin, must be differentiated from bog spavin (see following text). Tarsal tenosynovitis causes swelling both medially and laterally in the depression between the calcaneal tendon and the caudal aspect of the tibia (Figure 6-30). With severe effusion of the tarsal sheath, fluid distention can be palpated distal to the hock on the medial aspect. Thoroughpin usually is an incidental finding, seen most commonly in Western performance horses, but acute lameness accompanied by tarsal tenosynovitis can indicate strain or injury of the sheath, often associated with adjacent bony injury. Unusually, swelling in the distal, caudal aspect of the crus identical to that seen with classic thoroughpin is seen, but communication with and concomitant swelling of the tarsal sheath are absent. The term spavin refers to “any disease of the hock joint of horses in which enlargements occur, often causing lameness … the enlargement may be due to collection of fluids or to bony growth.”11 Bog spavin is fluid distention of the tarsocrural joint capsule. The tarsocrural joint has four outpouchings: dorsolateral, dorsomedial, plantarolateral, and plantaromedial. All joint pouches may be distended, although the dorsomedial and plantarolateral pouches are large and most prominent (Figure 6-31). With ballottement, fluid can be pushed between pouches on the dorsal or plantar aspects, thus differentiating this condition from thoroughpin. Bone spavin refers to fibrous and bony swelling that results from chronic osteoarthritis of the proximal intertarsal, centrodistal, and tarsometatarsal joints. This swelling

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Fig. 6-30  •  Thoroughpin, swelling located in the distal, caudal aspect of the crus, usually is caused by distention of the tarsal sheath and must be differentiated from effusion of the plantarolateral pouch of the tarsocrural joint (bog spavin).

Fig. 6-31  •  Moderate-to-severe tarsocrural effusion, bog spavin, in this draft filly was caused by osteochondritis dissecans of the cranial inter­ mediate ridge of the distal aspect of the tibia. Distention of the large dorsomedial pouch and swelling of the dorsolateral, plantarolateral, and plantaromedial pouches was present.

60

PART I  Diagnosis of Lameness Curb describes swelling along the distal, plantar aspect of the hock and has often erroneously been blamed on long plantar desmitis. In most horses the swelling is actually enlargement of the SDFT or subcutaneous tissues. The swelling is often firm, but in some horses subcutaneous fluid can be present (see Figure 78-1). In horses with acute severe injury the swelling may feel soft and mushy. In some normal horses the proximal aspect of the MtIV is prominent and should not be confused with curb. Swelling restricted to the medial or lateral aspect of the hock may reflect collateral ligament injury. Localized heat on the medial aspect of the hock or on the proximal aspect of the metatarsal region may be an important finding.

THE CHURCHILL HOCK TEST Dan L. Hawkins

Fig. 6-32  •  Bone spavin (arrows), fibrous and bony swelling on the medial aspect of the distal hock joint (left hindlimb) caused by chronic osteoarthritis of the distal hock joints, sometimes appears in older sports horses but is rare in young racehorses. The presence of bone spavin should be noted, and this area should be palpated carefully, but horses can have distal hock pain without bone spavin, and horses with bone spavin can have lameness elsewhere in the limb. Previous cunean tenectomy causes chronic fibrosis in this region.

usually is seen in older horses and can be palpated and observed on the medial side of the hock (Figure 6-32). Although the bony enlargement is the result of proliferation, it does not necessarily mean that the horse is lame as the result of the condition. Most horses with distal hock joint pain do not have palpable enlargement medially, and based on radiological evaluation, the most common area of proliferation and bony change is the dorsolateral aspect of the joints. Blood spavin is an old term usually meaning enlargement of the saphenous vein,3 but it also may have been used to describe a prominent saphenous vein in horses with bog spavin. Saphenous distention is rare, and the term is not used today. Occult or blind spavin is an obsolete term used to describe horses with clinical signs of hock lameness but no observable bony swelling.3 High spavin is also an obsolete term used to describe bone spavin located close to the tarsocrural joint.3

The Churchill hock test was developed by Dr. E.A. Churchill in the 1950s as a rapid, noninvasive, specific method to screen and identify distal tarsal pain in athletic horses. Although the test has been used by Dr. Churchill and me primarily in STBs, TBs, endurance horses, and Three Day Event horses, it is equally reliable when applied to other equine athletes. Digital pressure is applied on the plantar aspect of the head of the second metatarsal bone (MtII) and fused first and second tarsal bones with the limb in a non–weightbearing position. Abduction of the limb is a positive response. To examine the left tarsus, the clinician approaches the horse facing caudally. The left hindlimb is picked up and brought forward, supported by the clinician’s right hand cupped under the fetlock or hoof. Holding the limb so that the hoof is approximately 25 to 30 cm above the ground is most comfortable for the horse. The heel of the left hand is positioned on the proximodorsal surface of the third metatarsal bone (MtIII) while the third phalanges of the index and middle or middle and ring fingers are placed around the medial side of the tarsus to engage the bony ridge formed by the head of the MtII and the first and second tarsal bones (the area of insertion of the cunean tendon) (Figure 6-33). The thumb is rested on the dorsal lateral aspect of the tarsus and the proximal aspect of the MtIII. Gentle, firm pressure is applied to the bony ridge by flexing the phalanges of only the index and middle fingers (Figure 6-34). The hand does not squeeze the hock. Pressure is applied three times approximately 1 second apart, each time with increasing intensity to a maximum effort on the third time. Proficiency requires patience and routine practice. Consistent diagnostic information can be obtained safely from more than 90% of fit racehorses. If the limb cannot be picked up, the test cannot be performed. Fussing and repeatedly flexing the hock and limb in an agitated manner while the procedure is performed should not be misinterpreted as a positive response. The Churchill hock test is useful for horses that are not visibly lame but for which the trainer or rider has a complaint that the horse is doing something uncharacteristic during work or competition associated with decreased performance. The horse may have a changed attitude toward work, lugs in or out, is rough in the turns, refuses to change



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leads, stops at jumps, jumps to one side, or is stiff going in one direction. Although these horses cannot be blocked out at a slow gait, the Churchill hock test may suggest the presence of distal hock joint pain.

SAPHENOUS FILLING TIME Mike W. Ross The veterinarian should assess the saphenous vein filling time. Blood flow in the saphenous vein is prevented using digital compression in the proximal metatarsal region, and the blood accumulated in the vein over the tarsocrural joint is pushed proximally to completely collapse the vein. The finger compressing the vein distal to the hock is then removed, and the time it takes for the saphenous vein to fill is observed. Normally, it takes less than 1 second for the vein to fill, but in horses with reduced circulation, prolonged filling time is seen. Pulse quality of the dorsal metatarsal artery, located on the dorsolateral aspect of the MtIII just dorsal to the fourth metatarsal bone (MtIV), can be useful, especially if the history suggests lameness is caused by vascular compromise. The arterial pulse quality is compared with that in the contralateral limb. Fig. 6-33  •  Correct left hand placement in the left proximal metatarsal region to perform the Churchill hock test. (Courtesy Dan L. Hawkins, Gainesville, FL.)

Metatarsal Region

The veterinarian should palpate the digital flexor tendons and SL. Tendonitis is unusual in the hindlimb, but occasionally SDF tendonitis occurs in the proximal metatarsal region. This is most common in horses with curb, and tendonitis progresses distally to involve the metatarsal area. The hock angle is evaluated carefully. Occasionally horses with severe curb or those with SDF tendonitis of the metatarsal region have a reduced hock angle (obvious unilateral sickle-hocked conformation), indicating loss of support in the SDFT. Once a general palpation for the presence of heat, swelling, and exostoses associated with the MtIII, the MtII, the MtIV, and the proximal aspect of the DFTS has been completed, the limb is lifted and deep palpation is performed. The clinician should carefully palpate the origin and body of the SL, keeping in mind that both false-positive and false-negative responses can occur (Figure 6-35). Much of the palpation of the SL laterally is indirect, because the MtIV hides the origin and proximal aspect of the body. Because the presence of the splint bones and dense metatarsal fascia prevents substantial swelling, or at least the clinical recognition of swelling of the SL, even mild swelling in the proximal, medial metatarsal region should be carefully interpreted. With the limb in flexion, the axial borders of splint bones are palpated. The dorsal aspect of the MtIII should also be assessed with the limb in flexion, because bony injury of the MtIII does occur and includes dorsal cortical trauma from external injury or interference, dorsal cortical and spiral fractures, and proximal dorsolateral fractures.

Metatarsophalangeal Joint Fig. 6-34  •  The Churchill test is demonstrated on an anatomy specimen. The index and middle fingers are flexed and positioned on the bony ridge formed by the third metatarsal bone and the fused first and second tarsal bones, and the heel of the hand rests on the proximodorsal aspect of the third metatarsal bone. The thumb rests against the dorsolateral aspect of the tarsus. (Courtesy Dan L. Hawkins, Gainesville, FL.)

Many of the common problems of the metatarsophalangeal (MTP) joint, such as short, midsagittal fractures of the pro­ ximal phalanx, sesamoiditis, maladaptive or nonadaptive remodeling of the MtIII, and osteochondrosis, cause very few clinical signs, and although palpation is quite important, diagnostic analgesia is often needed to localize pain to

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PART I  Diagnosis of Lameness

Fig. 6-36  •  The metatarsophalangeal joint region often is overlooked during lameness examination. This joint should be palpated carefully with the limb in the standing and flexed (shown) positions. (Courtesy Ross Rich, Cave Creek, Arizona.)

Fig. 6-35  •  Deep palpation of the proximal aspect of the suspensory ligament can be performed only with the limb in flexion. The close association of the suspensory origin to the Churchill site explains the need to differentiate proximal plantar metatarsal pain from distal hock joint pain using diagnostic analgesia. (Courtesy Howard “Gene” Gill, Pine Bush, New York.)

this area. Nonetheless, careful palpation of the fetlock region is mandatory. Some horses have concurrent MTP joint and stifle pain, and when suspicious findings exist in one site, the veterinarian should look carefully at the other for additional, secondary, or complementary problems. The MTP or hind fetlock joint is evaluated with the limb bearing weight and in flexion. The clinician should assess the MTP joint capsule and the DFTS for the presence of effusion or fibrosis (Figure 6-36). Incidental effusion of both the MTP joint and the DFTS is common in the hindlimb of older performance horses; therefore this finding should not be overinterpreted. In younger horses, particularly racehorses, the presence of effusion can be an important clinical sign associated with osteoarthritis or other problems and should be interpreted accordingly. The clinician should carefully palpate for the presence of heat and mild swelling over the surface of both PSBs, subtle but important signs of sesamoiditis. Sesamoiditis is more prevalent in the hindlimb but can be difficult to detect, and advanced imaging often is necessary for diagnosis. The digital pulse amplitude should be assessed. With the fetlock joint in flexion, the veterinarian should palpate the proximal, dorsal aspect of the proximal

Fig. 6-37  •  Palpation of the proximal, dorsal aspect of the proximal phalanx can elicit pain in horses with incomplete mid-sagittal fracture of the proximal phalanx. In trotters, interference injury from the ipsilateral front foot causes pain and swelling in this region. (Courtesy Ross Rich, Cave Creek, Arizona.)

phalanx for the presence of pain or exostoses (Figure 6-37) and should apply pressure to the PSBs, avoiding aggressive compression, which may cause false-positive results. The range of motion of the MTP joint is noted.

Pastern

When the limb is elevated, the reciprocal apparatus causes constant flexion of the digit, which makes palpation of the



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plantar aspect of the pastern exceedingly difficult. Subtle swelling in the plantar aspect of the pastern is easy to miss. Bony and soft tissue structures should be palpated with the horse in the standing position, and the veterinarian should note the same clinically important areas that were pointed out for the forelimb. High and low ringbone (osteoarthritis of the proximal interphalangeal and distal interphalangeal joints, respectively), osteochondrosis of the pastern joint, and soft tissue problems such as SDF branch tendonitis, distal sesamoidean desmitis, and plantar injury of the pastern joint occur, but with reduced frequency when compared with the forelimb.

Foot

A similar approach to the evaluation of the hind foot as that described for the front foot is used. I spend considerably less time evaluating the hind foot than the front foot, unless the history or horse type dictates otherwise, because this area is relatively infrequently the source of pain. In the draft horse, hind foot pain is as common as in the forelimb, and therefore the hind feet merit considerable attention. Unless specifically indicated by the lameness history, or the horse is severely lame without an obvious cause in the upper limb, I do not routinely perform a hoof tester examination of the hind feet. Pressure with hoof testers over the frog and across the heel in a hind foot often causes a falsepositive response in normal horses. The position needed to perform an unassisted hoof tester examination in the hindlimb can be dangerous. The presence of an assistant to elevate the limb may obviate some of the risk. The examiner should assess the shape, balance, and contour of the foot and observe the shoe (or lack of one) carefully. Hoof angle in the hindlimb ranges from 48 to 58 degrees, and the hoof and pastern axis should be straight. A common finding is a low or underrun heel. An interesting relationship between a low heel and the presence of PSD has been noted.2 In these horses a lateral radiographic image of the foot shows that the plantar aspect of the distal phalanx is lower than the dorsal aspect.2 Shoe wear is extremely important in the hindlimb and can give clues to the source of lameness. For instance, horses with distal hock joint pain tend to stab the lower hindlimb during advancement, causing excessive wear of the lateral branch of the shoe (Figure 6-38). Other causes of lower hindlimb lameness, such as osteoarthritis of the MTP joint, can cause a similar gait, but usually abnormal shoe wear is less pronounced. Horses with stifle lameness often wear the medial branch of the shoe. The presence of heel and toe caulks or borium causes additional shear stress on many of the lower limb joints and can exacerbate lameness.

THE ROLE OF PHYSICAL EXAMINATION IN THE LAMENESS EXAMINATION Body temperature may assist with a clinical diagnosis. The normal temperature range is 37.5° to 38.6° C (99.5° to

Fig. 6-38  •  It is imperative to observe the hind shoes for wear during lameness examination. This right hind shoe (lateral is to the right) has wear along the dorsal and lateral aspects (lateral aspect of toe grab and fullering are worn) consistent with a lower hindlimb lameness, such as distal hock joint or proximal metatarsal region pain.

101.3° F), although in a foal the upper limit may normally be slightly higher. Body temperature in foals rises more abruptly than in adult horses in response to stress, infection, and inflammation. Thus transport of a foal may cause transient low-grade pyrexia, but fever in an adult horse after transport is abnormal. Localized infection in a foal usually causes pyrexia but rarely does so in an adult. The examiner should not exclude infectious arthritis in an adult horse simply because fever is not present. However, adult horses usually are pyrexic during the early stages of cellulitis or lymphangitis. Elevation in the pulse and respiratory rates often accompanies severe lameness because of pain. Systemic diseases such as endotoxemia may cause abnormal vital parameter findings in any horse and can lead to conditions such as laminitis. It is important to remember that diseases of other body systems can cause clinical signs that mimic lameness or cause true gait deficits. For instance, abnormal or stiff gaits can be seen in horses with pleuritis and peritonitis, abdominal, sublumbar, inguinal, thoracic inlet, and pectoral abscesses or tumors. Proliferative new bone associated with hypertrophic osteopathy may be associated with a thoracic or abdominal mass. If an unusual situation arises, the veterinarian should step back and think of the exception rather than the rule, because the “red herring” may be just around the corner.

PART I  Diagnosis of Lameness

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Chapter

7 

Movement Mike W. Ross

References on page 1256

“The best time for examining a lame horse is while he is in action. An attendant should lead him on a trot, preferably on hard ground, in a straight line, allowing him freedom of his head, so that his movements may all be natural and unconstrained.” A. Liautard, 18881

It would be difficult to improve on Liautard’s insistence that the lame horse be examined during movement or his description for how it is best accomplished. Although all parts of the lameness examination are important, the key is the determination of the limb or limbs involved. Not all horses with musculoskeletal problems exhibit lameness that is perceptible under normal conditions, or even by use of high-speed or slow-motion cinematography, gait analysis, or other sophisticated imaging devices. Under most circumstances, however, lameness from pain or a mechanical defect in gait is discernible, and the essence of the lameness examination is to determine the source of the pain. This discussion includes relevant experimental findings to support clinical observations, but sometimes experimental findings are confusing rather than informative.

GAIT Gait, defined as the “manner or style of walking”2 or “the manner of walking or stepping,”3 is used to describe the speed and characteristics of a horse in motion. The natural gaits, those exhibited when a horse is free in a field, are the walk, trot, and gallop.4 The canter is a collected gallop. Other gaits including the pace, running walk, rack (a singlefoot or broken amble), fox trot, and amble are artificial gaits, although some pacers pace “free-legged” (without the use of hobbles) while on the track, either at a slow speed or racing speed, and occasionally a Standardbred (STB) paces free-legged in a field. In some instances a trotter switches from a trot to the pace, but this change usually is exhibited while the horse is performing at speed and may be associated with lameness or interference. Lame trotters usually “make breaks,” going off stride, by switching (breaking) from the trot to the gallop. The term beat describes the number of foot strikes in a single stride cycle regardless of whether one or more feet strike the ground simultaneously. The following abbreviations are used for limbs: left forelimb (LF), right forelimb (RF), left hindlimb (LH), and right hindlimb (RH). The walk is a four-beat gait in which all four feet strike the ground independently without a period of suspension (in which no feet are on the ground). Depending on the part of the stride during which observations begin, the walk can appear to be lateral or diagonal. In general, in a lateral gait, both feet on one side strike the ground before the feet on

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the contralateral side. In a diagonal gait, one foot strike is followed by a strike of the foot located diagonal and contralateral to the initial foot (e.g., LF followed by the RH). Lame horses should always be evaluated at the walk. Stride length should be evaluated and compared with observations at the trot. Stride length and sequence of footfalls are easier to see while horses are walking than while they are trotting. Horses with hindlimb lameness may be examined for failure to track up.5 Horses normally track up, or overtrack. The hind foot is placed in or in front of the imprint of the ipsilateral front foot. Failure to track up usually is caused by hindlimb lameness or poor impulsion, and the hind foot imprint is seen behind that of the ipsilateral front foot.5 Although unusual, occasionally a horse will be observed to pace while walking, a finding that may indicate the presence of neurological disease. In breeds unassociated with the pace or similar gaits, young horses that pace should undergo careful neurological evaluation. Pacing while walking may be completely normal, and in older, “made” horses (horses that have already achieved an upper level of performance) the finding should not be overinterpreted. Backing is a diagonal, two-beat gait. Horses seldom back naturally, but backing commonly is required of horses during performance events, while exiting from a trailer, or while driving. Backing is useful during lameness examination to evaluate certain gait deficits, such as those associated with shivers, stringhalt, and neurological disease. The trot is a diagonal, theoretically two-beat gait, and diagonal pairs of limbs move simultaneously. The trot is theoretically a symmetrical gait, meaning both “halves” (beats) of the stride are identical, and at low speed in a sound horse, symmetry is likely achieved. However, at speed, perfect balance and fine management of weight (of the shoes) are necessary for a trotter to be perfectly symmetrical. There is a moment of suspension between impact of each diagonal pair of limbs. Some elite dressage horses do not have a two-beat gait but show advanced diagonal placement. This means that the hindlimb of a diagonal pair of limbs lands first and therefore is the only limb bearing weight. Hindlimb lameness is present in a higher percentage of horses that perform at speed at the trot compared with galloping horses because of differences in weight distribution in the trot and gallop. Compensatory lameness develops in the diagonal paired limb. LF lameness predisposes to RH lameness. Interference between limbs is more common in horses that trot at speed when compared with those that gallop. Likewise, hindlimb lameness is relatively common in dressage horses. The pace is a symmetrical, lateral, two-beat gait predominantly in STB racehorses and is characterized by movement of lateral pairs of limbs simultaneously (LH and LF; RH and RF), with a moment of suspension between lateral pairs. Pacers also have a high percentage of hindlimb lameness, but compensatory lameness usually develops in the lateral paired limb. RH lameness predisposes to RF lameness. The gallop or run is a four-beat gait. In the gallop and the canter the horse leads with the LF or RF, the forelimb that strikes the ground last in the stride sequence. An unrestrained horse usually leads with the LF while turning



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to the left, or the RF while turning to the right. Fatigue also plays a role. A Thoroughbred (TB) racehorse racing counterclockwise leads with the LF on the turns but immediately after entering the stretch switches to the right lead. Failure to switch leads or constantly switching leads in the gallop or canter may reflect fatigue or lameness. In a left lead gallop, the RH strikes the ground first, followed in sequence by the LH, RF, and LF, followed by a period of suspension. When a horse is on the right lead, the RF strikes the ground last, propelling the horse into the suspension phase of the stride. It is often assumed that a horse with RF lameness is reluctant to take the right lead. However, bone stress measured in the radius and the third metacarpal bone (McIII) is greater on the nonlead (trailing) forelimb, and thus a lame horse may change leads to protect the nonlead forelimb.6 Ground reaction forces (GRFs) are greater in the trailing (nonlead) forelimb, a fact that supports the clinical observation that horses with forelimb lameness may select leads to protect the lame forelimb. A horse with RF lameness may prefer the right lead, allowing the LF to assume the greater forces and bone stress.5 The canter (lope) is a three-beat gait. In left lead canter the RH strikes the ground first, then the LH and RF land simultaneously, followed by the LF and then a period of suspension. A horse reluctant to take a lead may be trying to compensate for hindlimb lameness. In the right lead the LH must absorb a considerable amount of concussion and then generate propulsive forces. Proneness of this limb to fatigue seems logical, but a consistent change in stride characteristics of fatigued horses to protect the LH was not seen.7 Although the LH strikes the ground first, stance time, flexion of the upper limb joints, and GRF are greater in the RH.5 It could be assumed that a horse lame in the RH would be reluctant to take the right lead and may prefer the left lead.5 Lead and stride characteristics of fatigued and lame horses are complex because of asymmetry of the gait, and forelimb and hindlimb problems could account for failure or reluctance to take a particular lead and inappropriate lead switching. Young horses early in training or trained horses that are lame may exhibit a disunited canter. The horse may spontaneously change legs behind, but not in front. In changing from left to right lead canter, or vice versa, the forelimbs and hindlimbs should change simultaneously. Horses with back pain or hindlimb lameness may be reluctant to change leads, or may change in front but not behind.

The Lameness Examination: Which Gait Is Best?

The trot is the most useful gait to determine the location of the lame limb or limbs. Forelimb lameness in particular is difficult to observe at the pace, especially in horses that are led in hand. Lame trotters may pace, supporting the supposition that the pace is an easier gait in a lame STB. I have seen horses with severe forelimb lameness at the trot that looked barely lame when pacing.

Comparing Lameness Seen at the Walk and Trot

Although lameness score should be determined when trotting a horse (see later), it is useful to compare gait deficits at the walk and trot. In horses with forelimb lameness, an exaggerated head and neck nod may be observed while

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walking horses with upper limb lameness (genuine shoulder region pain, for instance), and, in fact, head and neck excursion may be more pronounced than that seen while the horse is trotting. Some horses may exhibit odd gait deficits while walking, but deficits may abate at the trot. Horses with rare upper forelimb pain from rib fractures or anomalies may manifest abduction of the forelimb during protraction at the walk but not the trot. The stance phase of the stride is relatively longer at the walk than at the trot. The deep digital flexor tendon and the collateral ligaments of the distal interphalangeal joint are stressed maximally with extension of the distal interphalangeal joint. Thus with severe injuries of either structure lameness may be more severe at the walk than at the trot because of greater extension of the distal interphalangeal joint associated with the relatively long stance duration.5 Horses with hindlimb lameness characterized by a shortened caudal phase of the stride at the walk but shortened cranial phase at the trot often have upper limb lameness, such as that caused by pelvic fractures or osteoarthritis of the coxofemoral joint or from severe pain originating from the foot. In general, horses that have limb flight characteristics that differ between walk and trot should be evaluated carefully because in my experience they often have bona fide pain originating from the upper limb or are affected with an unusual mechanical or neuromuscular deficit.

Relevance of Lameness at a Trot in Hand

Is lameness seen at a trot in hand the same lameness that compromises performance at speed? Is the lameness seen at a trot in hand in a jumping horse the same problem that causes the horse to refuse fences? The answer is usually, but not invariably, yes. For instance, I have seen many STBs show subtle unilateral hindlimb lameness at a trot in hand, but when the horse was later examined at the track and hooked to a cart, pronounced contralateral hindlimb lameness was noted. Differences include the track surface, the act of pulling a cart, the additional weight of the driver, and a faster gait. Lameness often is evaluated on a smooth hard surface useful in exacerbating even subtle problems, but most horses perform on softer surfaces, when other problems may be apparent. More than one lameness problem may exist—one evident at a trot in hand and another while the horse is ridden or driven. Horses can show lameness from one problem when trotted in a straight line but lameness from an entirely different problem while being trotted in a circle. The answer to the first question is complex because performance itself entails the inextricably intertwined relationship between horse and rider or driver and the possible presence of compensatory and coexistent pain. Ideally, to evaluate the role of lameness on poor performance, horses would be evaluated at the speed, at the gait, and in the manner in which they perform, conditions that usually are not always possible to reproduce.

Horse Temperament and Lameness Examination

Safety of the handler, observers, and the horse must always be considered throughout a lameness examination, and with a difficult horse the examination may need to be modified, especially on cold, windy days. In some female horses and geldings, judicious use of the tranquilizer acetylpromazine (0.02 to 0.04 mg/kg intravenously [IV]) permits continuation of the examination. I avoid use of

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this tranquilizer in stallions, although the possibility of paraphimosis is remote. Low doses of sedatives such as xylazine can be used (0.15 to 0.30 mg/kg IV) in stallions or other horses but can produce mild ataxia. Detomidine may be a better choice than xylazine because the drug lasts longer, thus allowing diagnostic analgesic procedures to be performed.5 I try to avoid using tranquilization and sedation, although some clinicians use them frequently and report that lameness in most horses may be more pronounced and easier to observe. Mild muscle relaxation may reduce the tendency of the horse to guard the lame leg. Mild analgesic effects of sedatives may mask mild pain, and in racehorses care must be taken to avoid use of drugs that may cause a positive result in a drug screen. In big moving, exuberant Warmblood horses, especially dressage horses (particularly stallions), sedation may be essential to accurately assess lameness.5

Leading the Horse during Lameness Examination

The horse must be led with a loose lead shank so that it can move the head and neck freely. It is impossible to see a head nod in a fractious or excited horse that is held tightly. Use of a chain lead shank over the nose facilitates control but is resented by some horses, and use of a bridle with a lunge line attached may be preferable.5 Horses should move at a consistent speed, not too fast and not too slow. A lazy horse may need encouragement with a whip. Constantly changing speed can make assessment of lameness difficult, but occasionally, assessing a horse during deceleration may reveal useful information about the existence of subtle lameness.5 A horse may have to be trotted up and down many times. It is sometimes useful for the examiner to lead the horse to assess subtle forelimb lameness, because gait abnormalities may become more obvious.

Surface Characteristics and Lameness Examination

The horse should be examined on a smooth, flat surface. I prefer a hard surface, such as pavement or concrete that creates maximal concussion and may exacerbate subtle lameness. However, the clinical relevance of mild lameness seen on hard surfaces, especially on turns, should not be overinterpreted. Many horses that are actively competing successfully show mild lameness on hard surfaces; it is important to understand that the horse does not perform on a surface of pavement, and foot strike patterns and gait could be much improved if the horse performs on firm but forgiving surfaces. Crushed rock, cobblestone, deep sand, or undulating grassy areas and potentially dangerous slippery surfaces should be avoided. It is important that the surface be nonslip because some horses appear to lack confidence while moving on hard surfaces and alter the gait. In these situations, horses may shorten the stride for protection rather than from lameness.5 Horses with studs or caulks on the shoes may develop induced lameness unrelated to the baseline lameness when trotting on hard surfaces.5 Ideally the gait on hard and soft surfaces should be compared, to help differentiate soft tissue from bony problems. Horses with foot pain usually perform worse on a hard surface. Lameness from soft tissue injuries, such as suspensory desmitis or tendonitis, tends to be worse on soft

or deep ground. To evaluate lameness during transition from a hard to a soft surface and vice versa, a horse can be examined while circling on a lunge line in an area where both surfaces coexist side by side.5 Care must be taken to prevent the horse from slipping during this examination.

DETERMINATION, GRADING, AND CHARACTERIZATION OF LAMENESS Six basic steps are necessary to determine, grade, and characterize lameness. The clinician should determine the following: 1. Primary or baseline lameness or lamenesses 2. Possibility of involvement of more than one limb and presence of compensatory (coexistent) lameness 3. Classification of lameness as supporting, swinging, or mixed 4. Grading of lameness or lamenesses 5. Alteration of the cranial or caudal phase of the stride 6. Presence of abnormal limb flight The primary or baseline lameness is the gait abnormality before flexion or manipulative tests are used. The practitioner attempts to abolish baseline lameness using analgesic techniques. Lameness in more than one limb may complicate determination of the worst affected limb. It is important to trot a horse even if it is quite lame at a walk, unless an incomplete or stress fracture is suspected. A horse may take a short step with a limb at walk, or can appear very lame, but trot reasonably soundly. Horses with scratches (palmar or plantar pastern dermatitis) or superficial wounds in the palmar or plantar pastern may appear quite lame at walk but trot relatively well. A STB pacer may walk extremely shortly both in front and behind but pace or trot without lameness. However, only the degree of lameness usually differs between a walk and trot. A horse may appear sound at walk and trot in hand, but lameness may be apparent trotting in a circle, in hand or on the lunge, or while being ridden. This lameness now becomes the baseline lameness, and it is under these conditions that the results of diagnostic analgesia should be evaluated. The clinician should try to recognize if the horse has bilateral forelimb or hindlimb lameness that manifests as shortness of stride or poor hindlimb impulsion, or if concurrent forelimb and hindlimb lameness are present. Moderate-to-severe hindlimb lameness can mimic ipsilateral forelimb lameness, although ipsilateral forelimb and hindlimb lameness also occurs. In these horses the veterinarian should perform diagnostic analgesia in the hindlimb first.

Compensatory Lameness

Compensatory (secondary or complementary) lameness results from overloading of the other limbs as a result of a primary lameness. It must be differentiated from the stride-to-stride compensation by a horse to avoid interference injury because of a gait deficit, or lameness, or to shift weight (load) during examination. A compensatory problem develops as the result of predictable compensation a horse may make over time for a primary lameness in a single limb. However, a horse may compensate for lameness in one limb by shortening the stride in another, a stride-to-stride change in gait that is not the result of lameness. For instance, in



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some trotters with severe LF lameness, reluctance to extend the LF may induce a compensatory shortening of the cranial phase of the stride in the LH limb, creating what appears to be a hike in the LH. If the veterinarian looks only at the hindlimbs, LH lameness may be diagnosed. A trotter performing at speed with LF lameness is likely to develop compensatory lameness in the RF or RH but not in the LH. However, the horse may appear to be hiking (lame) in the LH to avoid interfering with the LF. Elimination of obvious unilateral forelimb lameness usually resolves an ipsilateral pelvic hike. Most horses with pronounced forelimb lameness examined at a trot in hand will have a concomitant shortening of the cranial phase of the stride in the contralateral hindlimb, giving the false impression of coexistent lameness in this limb and vice versa. Experimental results appear to support this clinical impression. In 6 of 10 horses with stance phase forelimb lameness, compensatory movements of horses created a false lameness in the contralateral hindlimb (see following text).8 Once forelimb lameness is abolished using diagnostic analgesia, the shortened cranial phase of the stride in the contralateral hindlimb will abate. It is often difficult to know which lameness came first, but it is important to understand how horses compensate for lameness and which limbs are at risk to develop compensatory problems. Compensatory problems range from obvious lameness to only mild palpable abnormalities that may still compromise performance. Several predictable patterns of compensatory lameness are possible; the most common is bilateral forelimb or hindlimb lameness. Horses with a specific lameness in one forelimb are at risk to develop the same condition in the opposite forelimb. This tendency may not always be compensation for the primary lameness but may reflect simultaneous injury or degeneration of bone or soft tissue of both limbs. Abnormal loading of forelimbs or hindlimbs, faulty bilateral conformation, and the same shoeing or foot conditions all likely contribute to bilateral, simultaneous lameness. In horses with bilateral lameness, eliminating lameness in one limb usually results in pronounced contralateral limb lameness. Bilateral lameness may affect both limbs equally, resulting in a short, choppy gait. The horse may be lame in one limb while being circled in one direction and lame in the contralateral limb in the opposite direction. Racehorses that gallop are most likely to develop compensatory lameness on the contralateral limb or the ipsilateral forelimb or hindlimb. A TB racehorse with a left metatarsophalangeal joint lameness is most likely to develop a similar problem in the RH but may also develop LF lameness. In a trotter the contralateral limb is most at risk, followed by the diagonal forelimb or hindlimb. If a trotter has a right carpal lameness, the left carpus should be examined carefully; compensatory lameness also may occur in the diagonal LH limb. In a pacer the ipsilateral forelimb or hindlimb should be considered after the contralateral limb. In a pacer with LH lameness the RH and LF are at risk. The most common compensatory lameness is the same problem in the contralateral limb. However, suspensory desmitis is a common compensatory problem in both the contralateral and other limbs. In a TB racehorse or a jumper with LF lameness, RF suspensory desmitis is common. Primary RH lameness may result in suspensory desmitis in

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the RF. It is logical that soft tissue structures are particularly vulnerable to the effects of overload. Superficial digital flexor tendonitis may develop secondary to a primary problem in the contralateral limb. In trotters a common pattern is primary carpal lameness and compensatory osteoarthritis of the medial femorotibial joint in the diagonal hindlimb, or vice versa. Compensatory lameness also can develop in the same limb. In horses with front foot lameness the suspensory ligament (SL) often is sore, and some horses have suspensory desmitis. In horses with lameness abolished by palmar digital analgesia, most with navicular syndrome, scintigraphic examination revealed increased radiopharmaceutical uptake (IRU) in the proximal palmar aspect of the McIII in 30% of horses, indicating possible abnormal loading of the proximal aspect of the SL (Figure 7-1).9 Complete resolution of lameness may not be achieved until high palmar analgesia is performed. Horses with primary metatarsophalangeal joint lameness often have associated ipsilateral stifle pain, or vice versa.10 Determination of the primary site of lameness may be difficult without use of diagnostic analgesia and observing that blocking one site abolishes the majority of lameness. This phenomenon may be most common in STBs, but I have recognized it in all types of sport horses and in TB racehorses.

Supporting, Swinging, and Mixed Lameness

Lameness has classically been divided into three categories in an attempt to characterize the motion associated with the lame leg and to assign a cause to the lameness condition. These categories are described and discussed, but I firmly believe that adequate characterization of most lameness conditions is impossible and may be unnecessary. Supporting limb lameness describes a lameness that results in pain during the weight-bearing phase of the stride. Most lameness conditions are of this type. Supporting limb lameness also has been referred to as stance phase lameness, but this term is inappropriate because the swing phase of the stride is also altered. Swinging limb lameness describes lameness that primarily affects the way the horse carries the lame limb. However, most horses with painful lameness conditions alter the swing phase of the stride in a typical and repeatable fashion, and it is difficult to make a clear separation between supporting and swinging limb lameness. Swinging limb lameness should be a term reserved for mechanical defects of gait, such as fibrotic myopathy, upward fixation of the patella, stringhalt, or other lameness conditions causing a mechanical restriction of gait. In these horses, lameness is manifested in the swing phase of the stride with no apparent pain. Unfortunately, the term swinging limb lameness often is used inappropriately to describe the gait deficit in horses with painful, supporting limb lameness. Lameness associated with osteochondrosis of the scapulohumeral joint is often described as a swinging limb lameness because of a markedly shortened cranial phase of the stride. Dramatic improvement in the shortened cranial phase of the stride can be achieved by diagnostic analgesia, eliminating pain associated with lameness. Thus the gait deficit is the direct result of pain, and no clear differentiation between supporting and swinging limb lameness can be made. Horses with painful forelimb lameness almost always

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B

C

Fig. 7-1  •  A, Lateral delayed-phase scintigraphic view showing focal, mild increased radiopharmaceutical uptake (IRU) of the navicular bone (bottom arrow) and proximal aspect of the third metacarpal bone (McIII; top arrow). Normal modeling is seen in the dorsal aspect of the proximal phalanx. B, Dorsal delayed-phase scintigraphic image, and C, dorsomedial-palmarolateral oblique xeroradiographic image of a dressage horse with lameness abolished by palmar digital analgesia. IRU of the medial aspect of the distal phalanx (bottom arrow) corresponds to the area of subchondral radiolucency seen in the xeroradiographic image (C, arrowhead). Note the focal area of mild IRU involving the proximal aspect of the McIII (top arrow, A and B). Abnormal loading of the suspensory ligament may occur as a compensatory problem in some horses with navicular syndrome or other sources of palmar foot pain.

shorten the cranial phase of the stride, although perhaps not to the extreme as in a horse with authentic scapulohumeral joint lameness. Horses with any painful hindlimb lameness consistently shorten the cranial phase of the stride, a reliable clinical indicator of which limb is affected, and when pain is abolished, the cranial phase (swing phase) of the stride improves (lengthens). Because the terminology is confusing and often erroneous, I prefer to avoid use of these terms and simply describe lameness as accurately as possible. For instance, describing a horse as grade 2 of 5 LF lame, with a marked shortening of the cranial phase of the stride reminiscent of other horses I have seen with shoulder region lameness, gives the most accurate and useful information. There is an erroneous tendency to equate a swinging limb lameness with one that is more evident when the lame limb is on the outside of a circle. Upper limb lameness is often presumed yet not confirmed by diagnostic analgesia. It is logical that if a horse is reluctant to swing a limb forward, the lameness may be most prominent when the lame limb is on the outside of a circle. However, many horses with painful weight-bearing lameness show more pronounced lameness with the limb on the outside of a circle, a finding that neither suggests that lameness originates from the upper limb nor indicates the presence of swinging limb lameness (see following text). The outer limbs must stretch further and cover a larger circumference circle than the inside limbs. Slight temporal differences in the stance and swing phases of the inside and outside limbs are necessary to maintain gait symmetry.5 Therefore the

stance phase of the stride may be relatively longer for the inside hindlimb, resulting in extension of the fetlock for a longer time and stress on the suspensory apparatus, whereas for the outside hindlimb covering a longer distance in the same time, there may be greater extension of the fetlock for a relatively short time, but still with stress on the suspensory apparatus. Thus pain associated with hindlimb proximal suspensory desmitis is worse in some horses with the lame or lamer limb on the inside of the circle, whereas with others lameness is accentuated with the lame limb on the outside of a circle. The results of cinematographic analysis of gait in lame horses seem to support reservation of the term swinging limb lameness for horses with authentic mechanical gait deficits, rather than those induced by painful lameness. In a horse with a supraglenoid tubercle fracture examined at a trot in hand, a marked decrease in the cranial phase of the stride (protraction) was observed, along with a marked head and neck nod. A markedly shortened stride could be equated with swinging leg lameness, but high-speed cinematography showed that the cranial and stance phases of the stride were shorter than in the sound limb.11 A horse with unilateral semitendinosus fibrotic myopathy had a shortened stride length and a shortened cranial phase of the stride, but the stance phase did not differ from that of the unaffected contralateral limb.12 In my experience, most lameness conditions can be considered mixed lameness, with changes in gait during weight bearing or the stance phase and during the swing phase of the stride. With the exception of mechanical

defects in gait, I have not been able to categorize the clinical characteristics of most lameness conditions into swinging or supporting limb types. However, it has been suggested that swinging limb lameness is caused by muscle injury; supporting limb lameness is caused by bone, tendon, and ligament injury; and mixed lameness is caused by joint, tendon sheath, and periosteal injury.13 A shortened cranial phase of the stride is a common characteristic in forelimb and hindlimb lameness and should not be considered pathognomonic for the location or type of lameness.

DETERMINING THE LOCATION OF LAMENESS The horse should be observed at both the walk and the trot from the front, behind, and side. I spend most of my time watching the horse move away and then back toward me. Medial-to-lateral limb flight and foot strike can be evaluated only from this perspective, although cranial and caudal aspects of the stride and fetlock drop (see following discussion) can be evaluated only from the side. Most important, evaluation of lameness from this perspective allows the veterinarian to use the horse as a frame of reference. I find it quite useful to evaluate forelimb lameness when the horse is traveling away from me and hindlimb lameness when the horse is traveling toward me. This perspective allows use of the horse’s top line to see a subtle head and neck nod or pelvic hike. Only by observing the horse from the side can the cranial and caudal phases of the stride be determined. When first learning to assess lameness from the side, a linear frame of reference, such as a fence or wall in the background, may be helpful to notice head nod and pelvic hike against an immovable background. Application of pieces of tape or other markers to the horse’s head or a fixed point on the pelvis can assist recognition of upward and downward movement of that body part. Independent observation of the forelimbs and hindlimbs is needed to understand whether a horse has forelimb or hindlimb lameness or a combination. These observations then are amalgamated to form a final clinical impression.

Recognition of Forelimb Lameness

Forelimb lameness often is easier to recognize than hindlimb lameness. Understanding the concept of the head nod is vital to the correct interpretation of equine lameness. The head and neck elevate or rise when the lame forelimb is bearing weight or hits the ground and nod down or fall when the sound forelimb hits the ground. “When the [forelimb] is the lame one, the movements of the foot and head occur somewhat in unison. When the lame foot is raised, the head is elevated, but only to fall when the sound leg is brought to a rest.”1 Some clinicians find it easier to appreciate the head nod down, whereas others find it easier to recognize elevation of the head. When slow-motion videotape of lame horses is evaluated, it is immediately obvious that the elevation of the head and neck is much easier to see than the head nod down. In slow motion the horse appears to be elevating the head and neck just before the lame limb hits the ground, and then, during the later portion of the support or stance phase, the head and neck nod down. In fact, in

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slow motion it is head and neck elevation from a baseline level and later settling of the head and neck (nod downward) that are seen. The head returns or settles to baseline, giving the distinct impression that the horse is unloading the lame limb rather than loading the sound limb. The head and neck nod occurs as the contralateral limb begins the support or stance phase. Both head elevation and falling are present, but head elevation is much easier to detect when it occurs in unison with the lame limb hitting the ground. It is likely that a combination of visual clues allows the clinician to decide the primary forelimb lameness. Quantification of lameness and description of the actions of the lame and compensatory limbs have been attempted using gait analysis systems. In horses with amphotericin-induced carpal lameness, head movements were the most consistent indicator of lameness, followed by sinusoidal motion, or a rising and falling action, of the head and withers.14 The motion of the lame limb was assessed, and a falling of the head and withers during the support phase of the lame limb was noted, contrary to clinical perception and evaluation of slow-motion videotape of lame horses. It was suggested that an uncoupling of the weight from the lame forelimb and a “free fall–like” phenomenon occurred during weight bearing.14 The problem with this description is that it considers only the lame limb and is confusing. When evaluating a lame horse, the observer sees both forelimbs. During the later portion of the support phase of the lame limb, the sound limb is in the later portion of the swing phase and beginning the support or stance phase. Thus the head and withers drop described experimentally appears to occur concomitantly with the sound limb hitting the ground. The observer perceives the early portion of the stance or support phase. In general, a good correlation between clinical evaluation of forelimb lameness and that described using motion analysis has been observed. There was complete agreement between clinical determination of location of forelimb lameness and that detected by motion analysis using a computerized three-dimensional motion measurement system. However, the degree of lameness differed in 6 of 29 horses.15 In a more recent study subjective forelimb lameness grades were significantly associated with kinetic parameters, and vertical force peak and impulse had the lowest coefficients of variations and highest correlations with subjective lameness score.16 In fact, kinetic parameters using GRFs measured by force plate analysis detected subclinical lameness not seen by a trained observer, a finding that may indicate that quantitative lameness analysis may be useful in horses with subtle lameness.16 The maximal vertical acceleration of the head was the best indicator of forelimb lameness.17 Although horses with forelimb lameness shifted weight in a caudal direction to the diagonal hindlimb, the amount of withers motion was minimal. The authors reasoned that the tremendous mobility of the head and neck, allowing the horse to asymmetrically elevate the neck and thus load the nonlame forelimb, accounted for the lack of withers movement and the horse’s adaptation to forelimb lameness.17 A similar compensatory ability is not present in the hindlimb. Vertical displacement of the tuber coxae and forward motion or translation of the pelvis occur in horses with hindlimb lameness, because a mechanism such as head and neck movement does not exist.17 In a computer-generated model of a trotting horse the

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dynamic effects of head and neck movement accounted for the majority of load shift to the contralateral forelimb and diagonal hindlimb in horses with unilateral forelimb lameness.18 Load shift and compensation by the diagonal hindlimb in horses with unilateral forelimb lameness lend support to the clinical findings of compensatory lameness in the diagonal limbs in trotters. Instrumented shoes have been used experimentally to study motion in horses by quantifying GRF but have had limited clinical use.19,20 Lack of correlation between an in-shoe system and force plate analysis was disappointing, and neither research nor clinical application of the system was recommended.21 Although these systems are not currently widely available, in the future these or similar systems may be useful to objectively assess lameness and the response to diagnostic analgesic techniques in clinical patients. A remote monitored sensor-based accelerometergyroscopic (A-G) system showed good correlation in horses with either forelimb or hindlimb lameness when compared with a video-based motion analysis system used in horses moving on a treadmill.22 Hindlimb lameness was consistently higher (in grade) using the A-G system, but the system yielded false-positive results in horses with concurrent forelimb lameness.22 However, for a skilled observer, direct observation of the horse may be more accurate than kinetic or kinematic analysis of gait when a horse is lame in more than one limb.5

the observed pelvic hike, but more important, it makes the lame side look lower than the sound side. This is why it is important to watch the entire pelvis as a unit rather than the individual sides of the “hips.” In most horses with hindlimb lameness, particularly those without a substantial tendency to drift away from the lame limb, the elevation of the pelvis (pelvic hike up) when the lame limb hits the ground surpasses that when the sound limb is weight bearing. This elevation can be seen readily in slow-motion videotape analysis, but it may not be as obvious during clinical examination. Observing horses with hindlimb lameness from the front as the horse trots toward you may be useful. This approach allows the pelvic hike to be seen clearly using the horse’s top line as a frame of reference. Subtle pelvic elevation is best seen from this perspective. The use of markers on a fixed part of the pelvis can help to identify asymmetry. Stride length characteristics, height of foot flight, sound, and fetlock drop are also helpful (see following text). Horses with bilateral hindlimb lameness may have a short, choppy gait that lacks impulsion, but they may have no pelvic hike. Other methods to exacerbate the baseline lameness should be performed, such as circling the horse at a trot in hand or while on a lunge line. Lameness may be accentuated when the lame or lamer limb is on the inside or outside of the circle (see following discussion).

Recognition of Hindlimb Lameness

Hindlimb Lameness Confused with Forelimb Lameness

Historically descriptions of hindlimb lameness have been confusing. An important principle in the recognition of hindlimb lameness is the concept of the pelvic hike or asymmetrical movement of the pelvis. This has also been termed hip hike, but I prefer the term pelvic hike because it accurately describes how the pelvis moves in a horse with unilateral hindlimb lameness. The entire pelvis, not just the lame side of the pelvis, appears to undergo elevation. Because the horse has two “hips” and only one pelvis, the term pelvic hike seems preferable. Pelvic hike is the vertical elevation of the pelvis when the lame limb is weight bearing. In other words, the pelvis “hikes” upward when the lame limb hits the ground and moves downward when the sound limb hits the ground. The “haunch settles downward when the sound leg touches the ground.…”1 Some clinicians find it easier to see the downward movement of the pelvis, on the side of the lame limb, rather than the pelvic hike.5 It may be simpler to determine which side has the most movement, rather than looking for either a hike or a drop.5 The clinician must keep in mind that the pelvic hike is the clinical impression of the change in height of the pelvis, not the absolute or measured height. It is the shifting of weight or load that occurs as the horse tries to reduce weight bearing (unload) in the lame limb and transfer weight (load) to the sound limb. The ease with which this can be seen depends on the horse’s tail carriage; in a horse with a tail set on high and that is also carried high, this may completely obscure movements of the pelvis. Another explanation for asymmetrical movement of the pelvis involves one of the protective or compensatory mechanisms used by the horse to assist in breakover and minimize load on the lame limb. Many horses with hindlimb lameness drift away from the lame limb toward the sound limb. Drifting may decrease the magnitude of

It is important to understand how a horse with unilateral hindlimb lameness modifies its gait so that hindlimb lameness can mimic forelimb lameness at the trot. When the lame hindlimb hits the ground, the horse shifts its weight cranially to transfer load away from the lame limb. This causes the head and neck to shift forward and nod down at the same time. The contralateral forelimb bears weight simultaneously with the lame hindlimb and the head nod coincides, thus mimicking lameness in the forelimb ipsilateral to the lame hindlimb. I find it difficult to distinguish clinical characteristics of a head and neck nod caused by forelimb lameness from that caused by ipsilateral hindlimb lameness. Some clinicians have suggested that the head and neck nod caused by ipsilateral hindlimb lameness is less vertical in nature and more forward and downward. Head and neck movement in horses with hindlimb lameness is not always observed. Horses generally must have prominent (>3 out of 5, see later grading discussion) hindlimb lameness before compensatory head and neck movement develops. However, two horses with very similar severity of hindlimb lameness may have different characteristics of movement, which will result in an associated head nod in one, but not in the other. At the pace, a lateral gait, LH lameness mimics RF lameness and RH lameness mimics LF lameness. Evaluation of the horse moving in circles may help to determine if a head nod is related to primary forelimb or hindlimb lameness. If a head nod is exacerbated but a hindlimb lameness is less obvious, then there is probably coexistent forelimb and hindlimb lameness. However if the head nod and hindlimb lameness remain similar or both appear worse, it is more likely that the head nod reflects a primary hindlimb lameness.



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Horses can have a head and neck nod at the trot caused by singular forelimb lameness, singular ipsilateral hindlimb lameness, or concurrent forelimb and ipsilateral hindlimb lameness. A prominent head nod is seen in horses with simultaneous LF and LH lameness. The examiner first must determine whether both limbs are affected. Problems arise because occasionally a horse with only LF lameness may shorten the LH stride at the trot, leading the veterinarian to question whether LH lameness also exists. More commonly, however, horses with only lameness in a single forelimb shorten the cranial phase of the stride of the contralateral hindlimb. Horses with only LH lameness can have a rather pronounced head nod, and thus the veterinarian may question the existence of LF lameness. Although a horse with LF lameness may have a compensatory shortened stride of the LH, in the absence of lameness a marked pelvic hike should not be present. A head nod consistent with LF lameness may be inappropriately severe to be caused by mild LH lameness. If a horse has simultaneous LF and LH lameness, it is essential to perform diagnostic analgesia in the hindlimb first, because moderate-to-severe hindlimb lameness produces head and neck nod that is not abolished unless the hindlimb lameness is resolved. Resolution of the pelvic hike and reduction in the head nod should be expected with resolution of the hindlimb lameness. Simultaneous lameness of a diagonal pair of limbs is less common than simultaneous ipsilateral lameness, except in trotters, because many horses perform at gaits that appear to induce compensatory lameness in the ipsilateral limbs. With simultaneous LH and RF lameness the head nod reflects the forelimb component, a mandatory clinical sign for perception of RF lameness. The horse may drift away from the LH with shortening of the cranial phase of the stride. The horse may have a short, choppy stride in the forelimbs and hindlimbs. The horse may have a rocking gait. It cannot shift weight or compensate from stride to stride in the usual manner and thus tends to rock back and forth from the hindlimbs to the forelimbs. Reasonable agreement generally exists between clinical recognition of hindlimb lameness and that found experimentally. The use of markers placed on each tuber coxae of 13 horses with unilateral hindlimb lameness showed a consistent increase in vertical displacement of the pelvis during early weight bearing of the lame limb.23 Although the rise and fall of the pelvis was readily apparent and occurred consistently with weight bearing of the lame and sound limbs, respectively, the absolute height of the pelvis on the lame side did not rise above that of the sound limb.23 These findings are consistent with my clinical impressions. A head nod down when the diagonal forelimb was bearing weight further confirmed clinical observations that hindlimb lameness can mimic lameness of the ipsilateral forelimb.23 In a kinematic study using a three-dimensional optoelectronic locomotion system, hip acceleration quotient increased in horses with hindlimb lameness.24 Vertical displacement corresponded to the pelvic hike up on the lame limb, with a simultaneous forward movement of the head and neck during the stance phase of the lame limb.24 Pelvic height differed significantly between sound and lame limbs in an experimental study using a custom-made heart-bar shoe to induce transient hindlimb lameness.25 Pelvic height was reaffirmed as an important indicator of hindlimb lameness, but

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exaggerated pelvic hike seen on the lame side was proposed to be caused by push-off from the sound limb and occurred immediately before weight bearing of the lame limb.25 The importance of weight support and asymmetrical dorsoventral hindlimb movement (pelvic hike) was reaffirmed in a study using continuous three-dimensional kinematic monitoring of movement of the tubera coxae.26 The hip (pelvic) hike seen on the lame side was found to be a rapid upward movement that led to an increased dorsoventral displacement.26 GRF has been measured in normal horses and those with forelimb and hindlimb lameness.27-30 GRF is reduced in the lame forelimb or hindlimb with compensation by the other limbs. In horses with unilateral forelimb lameness, decreased horizontal GRF in the lame limb is compensated for by increased GRF in the contralateral forelimb and ipsilateral hindlimb.31 Decreased vertical GRF in the lame limb is compensated for by increased vertical GRF in the contralateral forelimb during the swing phase of the lame limb, and increased vertical GRF in both the ipsilateral and contralateral hindlimbs during the stance phase of the lame limb.31 During unilateral hindlimb lameness the decreased GRF in the lame limb is compensated for by increased GRF in the contralateral hindlimb and the contralateral and ipsilateral forelimbs.31 These experimental data support the clinical impression that a lame horse adapts by shifting load to the contralateral limb or by shifting load in a caudal direction for forelimb lameness and in a cranial direction for hindlimb lameness. Kinetic gait analysis in horses with hindlimb lameness or spinal ataxia was recently studied using a force plate mounted in an examination aisle, a setup that may prove useful for clinical use during lameness examination.32 Horses with hindlimb lameness had significant differences from normal and ataxic horses and their own contralateral hindlimbs in vertical peak force, vertical force impulse, and coefficient of variance of vertical force peaks.32 Uniquely, investigators examined ataxic horses at the trot and found significant differences in lateral force peaks (lateral hindlimb movements) between normal horses and those affected with spinal ataxia.32

Bilaterally Symmetrical Forelimb or Hindlimb Lameness

Bilateral lameness is a common cause of poor performance and may go unrecognized without additional movement, such as circling, lunging, or riding. Horses with bilaterally symmetrical forelimb lameness may have a short, choppy gait when trotted in straight lines. Horses with hindlimb lameness may lack lift to the stride, have a subtle change of balance, or have reduced hindlimb impulsion.5 If bilaterally symmetrical lameness is suspected, the veterinarian should select one limb and begin diagnostic analgesia. Horses often show pronounced lameness in the contralateral limb when the source of pain is eliminated.

THE LAMENESS SCORE: QUANTIFICATION OF LAMENESS SEVERITY I believe it is important to have a standardized lameness scoring system that allows the clinician to quantify

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PART I  Diagnosis of Lameness

lameness within and between horses. Ideally it should be consistent worldwide, but currently a scale from 0 to 5 generally is used in North America, and a scale from 0 to 10 is often used in Europe. Definitions vary within the grading systems. The system adopted by the American Association of Equine Practitioners (AAEP) provides a framework.33 • Grade 1 lameness: difficult to observe and not consistently apparent regardless of circumstances (such as weight carrying, circling, inclines, hard surfaces) • Grade 2 lameness: difficult to observe at a walk or trotting a straight line but is consistently apparent under certain circumstances (such as weight carrying, circling, inclines, hard surfaces) • Grade 3 lameness: consistently observable at a trot under all circumstances • Grade 4 lameness: obvious lameness with marked nodding, hitching, or shortened stride • Grade 5 lameness: characterized by minimal weight bearing in motion or at rest and the inability to move The AAEP system is potentially confusing because it grades lameness at both the walk and trot. It does not account for a horse that has a shortened stride at walk but trots soundly. In my experience, many lame horses show consistently observable lameness at a trot and therefore would have to be given a score of at least 3, leaving only grades 3 and 4 for use in the majority of lame horses. Horses with bilateral lameness and a shortened stride but no obvious head nod or pelvic hike are difficult to score based on this system.5 It does not permit grading under different circumstances, such as straight lines, circles on the soft in each direction, and circles on the hard.5 An alternative lameness scoring system is listed in Box 7-1. Lameness is scored only with the horse at a trot, and the grading system is used most often to describe lameness at a trot in hand. The system is useful for both forelimb and hindlimb lameness and is based on a range of 0 (sound) BOX 7-1 

Lameness Scoring Lameness grades from 0 to 5 are based on observation of the horse at a trot in hand, in a straight line, on a firm or hard surface. 0 Sound. 1 Mild lameness observed while the horse is trotted in a straight line. When the lame forelimb strikes, a subtle head nod is observed; when the lame hindlimb strikes, a subtle pelvic hike occurs. The head nod and pelvic hike may be inconsistent at times. 2 Obvious lameness is observed. The head nod and pelvic hike are seen consistently, and excursion is several centimeters. 3 Pronounced head nod and pelvic hike of several centimeters are noted. If the horse has unilateral singular hindlimb lameness, a head and neck nod is seen when the diagonal forelimb strikes the ground (mimicking ipsilateral forelimb lameness). 4 Severe lameness with extreme head nod and pelvic hike is present. The horse can still be trotted, however. 5 The horse does not bear weight on the limb. If trotted, the horse carries the limb. Horses that are non–weight bearing at the walk or while standing should not be trotted.

to 5 (non–weight bearing). In this system, a horse with unilateral hindlimb lameness of grade 3 or worse would have a head nod that mimics ipsilateral forelimb lameness. This system has limitations because as discussed previously a horse with a moderately severe hindlimb lameness may or may not have an associated head nod, depending on the gait characteristics caused by the source and degree of pain.5 There is a practical difference between this scoring system and that put forth by the AAEP. A horse with lameness grade 1 in this modified scoring system would have a lameness grade of 2 to 3 in the AAEP system. The modified scoring system is more flexible and allows clear differentiation among most lameness conditions. However, it does not account for a bilaterally symmetrical gait abnormality and may be difficult to apply in a horse with lameness in more than one limb. Many horses evaluated for subtle lameness or poor performance have a score of 0 to 1 because consistent lameness is not observed. Use of half grades provides greater flexibility and supports adoption of a scoring system from 1 to 10, assuming 0 denotes soundness. A third system is to grade lameness independently at both the walk and trot and under different circumstances— straight lines, circles on the soft, circles on the hard, and ridden—using a relatively simple 9-point scale in which 0 is sound, 2 represents mild lameness, 4 represents moderate lameness, 6 represents severe lameness, and 8 represents non–weight-bearing lameness.5 This system takes account of the fact that a horse may appear lamer at the walk than at the trot.

LAMENESS DETECTION Fetlock Drop

Assessment of fetlock drop, or extension of the metacarpophalangeal and metatarsophalangeal joints, may be helpful in recognition of the lame limb. In general, the fetlock joint of the sound limb drops farther when this limb is weight bearing than does the fetlock joint of the lame limb, because the horse is attempting to spare the lame limb by increasing load in the sound limb. This may be easier to detect by video analysis than in a clinical situation and may be more recognizable at the walk than at a trot. However, in some horses with moderate or severe unilateral suspensory desmitis or tendonitis, the fetlock drops markedly on the lame limb when the horse is walking, but at a trot fetlock drop usually is more pronounced in the sound limb. With bilateral suspensory desmitis or severe tendonitis the fetlock may drop further in the lamer limb. In horses with chronic hindlimb suspensory desmitis excessive fetlock excursion on the affected side may falsely reduce pelvic excursion (hike) and make hindlimb lameness less obvious and more difficult to detect.

Use of Sound

Sound can be useful in lameness evaluation. A lame horse usually lands harder on the sound limb, resulting in a louder noise. For this sound to be appreciated, the horse must be trotted on a firm or hard surface such as pavement or concrete. However, the sound a horse makes while landing depends greatly on symmetry of the front or hind feet, and the loss of one shoe, different shoe types, or disparity in foot size confounds interpretation. Listening for regularity of rhythm and sound of footfall are important, especially



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when evaluating the response of lame horses to diagnostic analgesia, particularly in horses with subtle lameness.5

Drifting

Horses with hindlimb lameness generally drift away from the lame limb. Drifting is one of the earliest adaptive responses of a horse with unilateral hindlimb lameness, allowing the horse to break over more easily or to reduce load bearing. Drifting may alleviate the need for extensive pelvic excursion (hike). It may make pelvic drop on the lame side more obvious. The horse may mask the lameness by reducing pelvic excursion. In some horses a pelvic hike is undetectable or subtle, but consistent drifting away from the lame side indicates the presence of hindlimb lameness. Many driven STBs with hindlimb lameness drift away from the lame limb or are “on the shaft.” Horses with LH lameness have a tendency to be on the right shaft and vice versa. Drifting away from the lame limb may be most evident when horses have pain from the tarsus distally, although some clinicians have different experiences.5 Drifting may result in the horse moving on three tracks. Horses with severe forelimb lameness also tend to drift away from the lame limb, but this tendency usually is less obvious than in horses with hindlimb lameness. Drifting is most common with carpal lameness when the horse tends to abduct the limb during the swing phase of the stride and appears to push off with the limb, forcing the horse away from the lame side. Abduction seen in horses with carpal lameness should not be confused with swinging the limb or a swinging limb lameness. During protraction abduction seen in horses with carpal region pain appears to involve the horse carrying and placing the limb lateral to the expected site of limb placement. Racehorses with either forelimb or hindlimb lameness tend to drift away from the lame limb while training or racing at speed. This finding is an important piece of the lameness anamnesis. Drifting toward the lame hindlimb is an unusual but important clinical sign. In horses that drift toward the lame limb, I suspect weakness and lameness exist simultaneously, suggesting a neurological component to the gait abnormality. However, a jumping horse at takeoff may push off more strongly with the nonlame hindlimb and drift across the fence toward the lame limb.5

EVALUATION OF LIMB FLIGHT Observation and characterization of limb flight can be useful in determining the lame limb or limbs and possibly the location of pain within the limb. Abnormal limb flight also may predispose to lameness, especially in horses with faulty conformation. In my opinion, it is impossible to predict the site of pain causing lameness accurately based solely on limb flight and other characteristics, although some abnormalities lead to a high index of suspicion. I believe strongly that the location of pain should always be confirmed by using diagnostic analgesic techniques whenever possible. Some abnormalities are consistently associated with specific lameness conditions, whereas others are general patterns of limb flight seen with many different conditions.

Cranial and Caudal Phases of the Stride

Changes in limb flight in the cranial and caudal phases of the stride can be seen only when the horse is evaluated

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from the side. In a normal horse the length of the stride of the paired forelimbs and hindlimbs, measured from hoof imprint to hoof imprint, is nearly identical from side to side. Extension and flexion of the limbs is also similar. From a clinical perspective the length of the stride of the affected limb cranial to the stance position of the contralateral limb is called the cranial phase of the stride, and the length of the stride caudal to the stance position of the contralateral limb is called the caudal phase of the stride. Obviously in a normal horse these individual parts of the stride are symmetrical. In a lame horse the overall stride length does not appear to change. If stride length changed, the horse could not trot in a straight line. Drifting is associated with lameness and could be explained by a change in stride length, but shorter stride length would be expected in the lame limb, causing the horse to drift toward the lame side, in contrast to the usual observation, drifting away from the lame limb. In racehorses, some of the tendency to drift away or toward the inside of the track could be easily explained by mild differences in stride length or strength (power). However, with the horse at a trot in hand we can assume that total stride length does not change. In most lame horses the cranial phase of the stride of the affected limb is shortened. The caudal phase is lengthened to maintain a near equal overall stride length side to side. Shortening of the cranial phase of the stride appears to be a learned response of the horse to reduce the time spent during the stance phase and to help during breakover. Loss of propulsion, or an unwillingness to push off with the lame limb, could also explain reduction in the cranial phase of the stride. Because most lame horses have a shortened cranial phase of the stride, this finding, although quite useful in determining in which limb the horse is lame, is not particularly useful in localizing or classifying lameness and is not synonymous with swinging limb lameness. It is also important to recognize that pain causing lameness results in altered proprioceptive responses, to protect the painful area, and these responses may persist for some time after pain has resolved.5 A classic example of attenuation of the cranial phase of the stride in the hindlimbs occurs mechanically in horses with fibrotic myopathy. This authentic swinging limb lameness causes a marked abrupt change in the later portion of the protraction phase of the affected hindlimb, shortening the cranial phase and causing a sudden downward and backward action of the limb. The caudal phase of the stride is lengthened in most lame horses because for overall equal stride length to be maintained, this portion of the stride must compensate. I generally have not found evaluation of the caudal phase of the stride at the trot in hand clinically useful, but it is sometimes a useful observation in horses at a walk (see following text). Some horses with severe palmar foot pain have a shortened caudal phase of the stride at both walk and trot.5 Contrast of the cranial and caudal phases of the stride in the lame limb at a walk and a trot is useful. In most horses with forelimb lameness the cranial phase of the stride is slightly shortened at a walk but markedly shortened at a trot. Obviously, in horses with subtle lameness, this clinical sign is absent at the walk and only mildly apparent at the trot. Horses with pain in the dorsal aspect of the foot, such as hoof abscessation or laminitis, may

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PART I  Diagnosis of Lameness

have a shortened caudal phase of the stride at a walk. This response is an attempt to protect the painful area and to shorten during breakover. These horses walk with a marked camped-out appearance in the forelimbs. At the trot, however, the cranial phase of the stride is likely to be shortened, a clinical contrast useful in localizing lameness to the dorsal aspect of the hoof. Most horses with hindlimb lameness have a reduction in the cranial phase of the stride at the walk and the trot. Horses with pelvic fractures involving the acetabulum prefer to keep the lame limb ahead of the contralateral limb at the walk and have marked shortening of the caudal phase of the stride, but at the trot the horse has a shortened cranial phase of the stride. Horses with hoof abscessation, most commonly of the dorsal aspect of the hoof, walk similarly, only to trot with a pronounced shortening of the cranial phase of the stride. An explanation for disparity at walk and trot in the phases of the stride in horses with pain at either end of the hindlimb is not readily apparent, but recognition of this phenomena has been quite useful, and consistent. Unilateral or bilateral laminitis and other severe causes of pain in the digit are rare in the hindlimbs and can cause similar clinical signs. Shortening of the cranial phase of the stride does not always indicate that lameness is present in that limb. At speed a trotter with forelimb lameness shortens the cranial phase of the stride in the ipsilateral hindlimb to avoid interference with the lame limb. This observation sometimes is also made in horses being trotted in hand. This compensatory movement gives the impression that the horse may be lame in the ipsilateral hindlimb, with a subtle pelvic hike. Lameness of the foot and carpus in trotters most often causes this compensatory ipsilateral hindlimb pelvic hike. Once lameness has been abolished in the ipsilateral forelimb, the subtle pelvic hike and shortened cranial phase of the stride in the hindlimb abate. In trotters a shortened cranial phase of the stride and a pelvic hike may be related to faulty weight distribution and interference problems and not to lameness at all.

ABNORMALITIES OF LIMB FLIGHT Abnormalities of limb flight can cause interference of one limb with another, particularly in trotters and pacers (Figure 7-2). However, horses performing at speed at any gait and those with faulty conformation also are at risk to develop interference injuries. In some horses, interference is of no consequence, but in others, especially trotters, it causes gait deficits. Skin lacerations, bruising, and underlying bone and soft tissue damage (interference injury) may occur. Various boots and other protective devices have been developed to protect the limbs from potential trauma. It is important to assess the presence and location of interference injuries. In some horses, only mild evidence of hitting is found, but other horses may have many painful areas. Chronic interference can be the sole reason for lameness or poor performance.

Front Foot Interference Front Foot Hitting the Contralateral Forelimb

Horses with toed-out conformation tend to wing in during movement, predisposing to interference injuries.

Trotter

A

B Pacer

D

C Fig. 7-2  •  Types of interference. A, Horses at any gait can be injured by interference of a forelimb with the opposite side. B, Interference is common in the trotter and usually involves the ipsilateral forelimb and hindlimb. Interference within a forelimb can be seen in horses that hit the elbow of the same limb. This usually occurs because of high action, excessive weight of the shoes, or a combination of these factors. C, Interference in the pacer can involve the forelimb and diagonal hindlimb, commonly called crossfiring. D, Forging occurs during trotting when the toe of the hind foot strikes the bottom of the ipsilateral front foot.

Horses with base-narrow conformation or those with a combination of base-narrow and toed-out conformation also are at risk. However, many horses with these conformational abnormalities do not interfere. Some horses walk very closely but widen out at faster gaits. Interference injury from one hind foot hitting the medial side of the contralateral hindlimb occurs infrequently. All types of horses, especially STB racehorses, are at risk for interference. Interference can involve any level of the limb from the foot to the proximal antebrachium. Mild interference of this type is called brushing. STBs often “hit their knees,” which causes swelling, bruising, and lacerations of the skin on the distal medial aspect of the radius. In some horses, large, chronic swellings develop; these consist of mostly fibrous tissue. In others, osteitis of the distal radius or abscessation occurs. Even with protective gear, horses may be reluctant to perform at maximal speed to avoid injury or disruption of gait, or pain caused by interference induces the horse to go off stride.

Interference within the Same Limb

Horses can develop interference injuries within a limb when the hoof or shoe hits the ipsilateral elbow. This type of interference sometimes is seen in trotters with high action (excessive carpal flexion) and is common in gaited horses that perform with heavy shoes intended to cause high action of the forelimbs (see Figure 7-2, B).

Front Foot Hitting the Ipsilateral Hindlimb

Interference in trotters usually involves the toe of a forelimb interfering with (hitting) the dorsal aspect of the ipsilateral hindlimb (see Figure 7-2). Various names are



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given to the type of interference based on the location in which the injury occurs. Interference injury at the dorsal aspect of the hind foot or coronary band is called scalping; in the pastern region it is called speedy cutting; in the metatarsal region (shin) it is called shin-hitting; and in the dorsal or medial aspect of the tarsus, it is called hock-hitting. Because interference is common in trotters, it is important not to overinterpret signs of pain on palpation. Speedy cutting results in pain over the dorsal aspect of the proximal phalanx that should not be misinterpreted as pain associated with a midsagittal fracture.

Front Foot Hitting the Contralateral (the Diagonal) Hindlimb

Cross-firing, or the striking of the contralateral (diagonal) hindlimb by the front foot, usually occurs only in pacers (see Figure 7-2, C).

Hind Foot Interference

Interference as a result of a hind foot hitting the foot of the ipsilateral forelimb (forging) is common and usually does not result in injury. Many horses forge at a trot in hand or while being ridden. In horses with shoes the sound is unavoidable but may not be a sign of a pathological condition. Forging is most common in horses that are trotted in deep footing. Forging may reflect imbalance, lack of strength, incoordination, or poor foot trimming.5

Forelimb: Common Abnormalities of Limb Flight Winging In and Winging Out

Common limb flights observed during lameness examination include winging in and winging out movement of the front feet and are often related to conformation (see Figure 4-13). Horses that are toed out tend to wing in, whereas those that are toed in tend to wing out. Such abnormalities do not necessarily compromise performance. However, such movement may result in uneven loading of the soft tissue structures and uneven hoof wear, leading to chronic imbalance. Horses that wing in tend to develop interference injuries and wear the medial aspect of the shoe excessively. Horses that wing out tend to develop lateral branch suspensory desmitis and wear the lateral aspect of the shoe excessively.

Lateral Placement of the Foot during Advancement (Abduction)

Horses normally advance the forelimbs straight ahead. When advancing the limb, horses with articular carpal pain, and some horses with pain in the proximal metacarpal region, place the foot lateral to the expected foot position. This action has been described as abduction of the limb, but this term may infer swinging the limb, and horses with carpal lameness seem to place the limb laterally rather than swinging the limb. However, ankylosis associated with severe osteoarthritis or arthrodesis of the carpus does necessitate swinging the limb during advancement, a much different movement from that seen in horses with more mild carpal region pain. Horses with this abnormality of flight almost always have a shortened cranial phase of the stride. They tend to push off with the affected limb from the lateral location, resulting in a wide or peg leg type of motion at walk, and sometimes at trot. With bilateral carpal lameness the horse appears to move widely bilaterally. Not all horses with

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carpal pain move widely, and this gait change is seen more often in horses with middle carpal or carpometacarpal joint pain than in those with pain in the antebrachiocarpal joint. Some horses with upper limb lameness may carry the limb widely while walking, although this characteristic is not typical of horses with shoulder pain. A horse with a humeral stress fracture sometimes may travel widely, similar to a horse with carpal lameness, but the latter is more likely. A horse with pain in the lateral aspect of a foot may move widely in the affected limb to reduce load laterally. This characteristic is seen in STB and TB racehorses with subchondral bone trauma or early stress fractures of the distal phalanx.

Plaiting

The verb to plait means to braid or pleat, or to make something by braiding.3 The term is used to describe horses that walk or trot by placing one foot directly ahead of the other foot. Plaiting in the forelimbs is not nearly as common as in the hindlimbs and usually is the result of base-narrow, toed-out conformation. Old horses (usually broodmares) with severe carpus osteoarthritis and carpus varus limb deformities occasionally may swing the limb laterally and place the foot far enough medially to end up in front of, or lateral to, the opposite foot. Some horses with shoulder region lameness guard the limb and travel very closely in front. Plaiting in the forelimbs can be seen in horses with recent fractures of the thoracic dorsal spinous processes at the withers.5 Horses with neurological disease occasionally plait.

Limb Flight in Horses with Shoulder Region Lameness

I include this section principally because the shoulder often is erroneously incriminated as the source of pain. Horses with moderate-to-severe lameness of the scapulohumeral joint or bicipital bursa have a marked shortening of the cranial phase of the stride. They also have an unusual motion of the shoulder joint that is difficult to describe. Because the cranial phase of the stride is shortened, during breakover the affected shoulder joint seems to drop or buckle forward, more so than the opposite side (assuming lameness is unilateral). There may be prominent lifting of the head and neck. Limb flight is either straight ahead or somewhat close to the opposite forelimb. Horses with shoulder region pain do not consistently travel widely, or abduct the affected limb. However, racehorses with humeral stress fractures may occasionally travel widely in front. With mild lameness there are no typical gait characteristics.

Hindlimb: Common Abnormalities of Limb Flight Stabbing or “Stabby” Hindlimb Gait

A common abnormality of limb flight seen in horses with hindlimb lameness is described as a stabbing or “stabby” gait. During protraction of the lame hindlimb or hindlimbs, the limb travels medially, close to the opposite hindlimb, and then moves laterally during the later portion of the swing phase and is placed lateral to the expected foot placement. This motion results in excessive wear of the lateral or dorsolateral aspects of the shoe. Although this gait often is seen in horses with distal hock joint pain, it can be seen with many other sites of pain from the distal tibia to the

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foot. Therefore diagnostic analgesia is required to localize the pain. However, horses with the most marked shoe wear consistent with this abnormality of limb flight are most likely to have tarsal lameness. Exaggerated stabbing hindlimb motion often is seen in horses with neurological disease.

Abduction of the Hindlimbs during Advancement

In some horses with hindlimb lameness the limb is carried forward in a position lateral to the expected position (i.e., abducted). In some horses with this limb flight the limb swings outside the expected line of limb flight, only to strike the ground near the expected position. Lateral swinging of the limb begins immediately after the lame limb leaves the ground. I have observed this abnormality most consistently in horses with stifle lameness, but it also occurs with some other upper limb lameness conditions. Care must be taken when evaluating horses that normally travel widely behind, such as trotters. I have recognized lateral swinging of the hindlimb most commonly in pacers with articular lesions of the stifle, because the normal gait in these horses is to swing the hindlimb more than would be expected from other horses. Many horses with stifle lameness carry the limb forward lateral to the expected position, but just before impact may actually stab laterally. Therefore the veterinarian must pay close attention to limb flight directly after the lame limb leaves the ground and while it is passing the contralateral limb. Another common characteristic of horses with stifle lameness is a shortened cranial phase of the stride. The stifle joint also may appear unusually prominent and be carried somewhat away from the flank and slightly externally rotated.

Plaiting

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PART I  Diagnosis of Lameness

Plaiting is more common in the hindlimb than in the forelimb and usually results from lameness rather than faulty conformation, although plaiting can occur in a horse with severe base-narrow conformation. Plaiting can be seen in horses with unilateral or bilateral lameness. In horses with unilateral lameness, it appears that limb flight actually may be altered in both hindlimbs, resulting in both hind feet being placed ahead, or in some horses, lateral to the opposite foot. In horses with severe hindlimb lameness, it appears that the affected foot is being swung around and placed directly in front or lateral to the unaffected foot. Alternatively, the horse may be trying to support most of its weight on the unaffected limb and moves this limb inside to support the lame side. In horses with bilateral lameness, it is equally difficult to determine what exactly is causing the plaiting. The horse may be reluctant to bring either hindlimb along the expected line of flight, leaving the limb medially and forcing the opposite limb to the outside to avoid interference. A horse may swing each hindlimb around the other, ultimately ending placing one foot ahead or lateral to the other. An unusual rocking type of gait is observed in horses with bilateral hindlimb lameness and plaiting. I have observed plaiting most commonly in horses with osteoarthritis of the coxofemoral joint or pelvic fractures, but I also have seen it in horses with bilateral distal hock joint pain or suspensory desmitis. Plaiting also is observed in some horses with sacroiliac joint pain.5

Mechanical Lameness of the Hindlimb and Limb Flight Mechanical conditions of the hindlimb can cause profound abnormalities of limb flight (see Chapter 48). These are termed lameness conditions because of the gait abnormality exhibited, although in many horses pain is not characteristic.

Stringhalt

Stringhalt, an ill-defined neuromuscular disorder of the hindlimb, causes mild-to-severe hyperflexion of the tarsus. The condition can be unilateral or bilateral and usually is most obvious at a walk but can also be seen at the trot. In horses with severe stringhalt the dorsal aspect of the hoof comes close to or hits the ventral aspect of the abdomen. Horses may exhibit the clinical signs more prominently during backing or when initially moved after previous standing.

Fibrotic Myopathy

Fibrotic myopathy is characterized by a sudden downward and backward motion of the limb (slapping motion) that occurs during, and restricts the length of, the cranial phase of the stride. Hyperflexion of the hock is not a clinical feature of this gait deficit, but the restriction of the cranial phase of the stride and the slapping motion and sound can be confused with the clinical signs of stringhalt. It is most obvious at a walk.

Upward Fixation of the Patella

Upward fixation of the patella is a classic hindlimb gait deficit and one that displays the function of the stay or reciprocal apparatus. It can be intermittent or permanent and unilateral or bilateral. When the patella is locked in position over the medial trochlear ridge of the femur, the stifle and hock joints are held in extension, whereas the digit is held in partial flexion.

Shivers

Shivers is an ill-defined neuromuscular disease and is most common in Warmbloods and draft breeds; it can occur unilaterally or bilaterally. Clinical signs usually are most obvious when a horse is backed or first moves from the stall. Horses elevate and abduct the limb, and the limb may actually shiver or shake. The tail often is elevated. Signs may be accentuated if the horse is tense.

Other Hindlimb Gait Deficits

Other unusual unexplained gait deficits affecting one or both hindlimbs are observed occasionally, and they often have characteristics similar to those seen with stringhalt, fibrotic myopathy, upward fixation of the patella, and shivers. However, some distinction usually prevents easy recognition and diagnosis. A gait deficit characterized by marked hindlimb abduction seen most prominently at the walk has been recognized. This is most similar to fibrotic myopathy, because a consistent abduction of the limb is observed, and signs tend to abate when the horse is trotted. It may be related to scarring, abnormal function of the biceps femoris and gluteal muscles, or neurological disease. Neurological disease can cause many different gait deficits, most commonly recognized in the hindlimbs but also in forelimbs. A complete neurological evaluation usually is



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not performed during lameness examination unless certain abnormalities are observed. Abnormal or excessive circumduction of the hindlimbs, a bouncy, stabby hindlimb gait noticed when the horse is trotted, knuckling over behind or crouching, stumbling, and lethargy are signs that should prompt further investigation.

EVALUATION OF FOOT PLACEMENT It is important to critically evaluate foot placement. Ideally, both the front and hind feet should land flat and level on a firm surface. Foot strike patterns change on soft footing. Evaluation of foot strike is most important in horses with lameness localized to the foot, but it can also give clues regarding other causes of lameness. Abnormal foot placement can be the result of a current lameness problem but may also cause lameness. In the forelimbs, horses commonly land on the lateral side of the foot first before rocking medially. This can be the result of abnormal conformation or hoof imbalance and can predispose to lameness in the digit and suspensory branch desmitis. Landing abnormalities in the dorsal-topalmar direction are common but are difficult to recognize unless severe. Horses with profound pain in the toe caused by laminitis or hoof abscessation land heel first, giving a camped-out appearance, and have a shortened caudal phase of the stride. Horses with palmar foot pain may compensate by landing toe first, causing abnormal stress on the dorsal structures of the foot, but this characteristic is difficult to see except in slow motion. In the hindlimbs, several patterns of abnormal landing or motion are recognized, not all of which are a cause or result of lameness. Landing on the toe is commonly considered the result of heel pain, but many horses with severe hindlimb lameness land on the toe. This tendency is particularly prominent when the horse is first moved, and most horses warm out of the lameness. Horses may land on the toe when walking up an incline or at the walk on the flat but generally place the heel on the ground when trotted. The most consistent lameness I see in horses that land on the toe is distal hock joint pain, but any cause of lameness from the tarsus to the foot can cause a horse to exhibit this abnormal landing pattern. Horses with lameness of the metatarsophalangeal joint region, including osteoarthritis, tenosynovitis of the digital flexor tendon sheath, or desmitis of the accessory ligament of the deep digital flexor tendon have a tendency to land on the toe. Horses with adhesions within the digital flexor tendon sheath may have severe mechanical restriction that causes toe-first landing. Old Western performance horses with deep digital flexor tendonitis have severe toe-first landing and may stand on the toe and even rise up in the heels during the examination. The condition can be bilateral or unilateral and is difficult to manage. Mild or moderate tendency to land on the toe also has been attributed to stifle lameness.5 Abnormal movement of the lower or entire hindlimb occasionally is noted when horses are watched from behind. Horses may place one or both hind feet in an axial position and collapse or break over the lateral aspect of the fetlock region.5 Another uncommon hindlimb motion is characterized by excessive rotation of the hindlimb. The horse plants the hind foot and rotates the heel laterally, causing abnormal loading or twisting of the distal limb.5

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Although this movement can lead to lameness, it sometimes is seen in horses that are successful in various sporting endeavors. I have seen this type of hindlimb motion most often in TB racehorses.

ADDITIONAL MOVEMENT DURING LAMENESS EXAMINATION Further information about the character of lameness often can be obtained by observing the horse as it moves in circles and is ridden or driven. Some lameness conditions are apparent only under these circumstances.

Hard and Soft Surfaces

Comparison of movement on hard and soft surfaces is valuable. Foot lameness usually is worse when the horse is trotted on hard surfaces and better on a soft surface, such as grass or sand. Horses with suspensory desmitis or digital flexor tendonitis are more likely to show lameness on a soft surface. Deep sand may accentuate some lameness conditions, but an extended lameness examination under these conditions could cause proximal suspensory desmitis.5 A slight downward incline or an uneven, rough surface may make subtle lameness more apparent.5

Circling

Lameness often is much more pronounced when a horse is circled. Horses should be circled in both directions: to the left (counterclockwise, LF and LH on the inside) and to the right (clockwise, RF and RH on the inside). Lameness may be more pronounced when circling at either the walk or the trot. In some horses with incomplete fractures, baseline lameness at a trot in straight lines in hand may be subtle or absent. Lameness may be readily apparent during circling, even at the walk. The additional forces of torsion and bending during circling are added to those of compression and tension. In horses with incomplete fractures, such as those involving the proximal or distal phalanges, torsion or bending forces during circling likely cause mild separation of the fracture fragments and exacerbate lameness. In horses with other lameness conditions, exacerbation of lameness may be caused by a change of load on the affected soft tissue structure or bone, redistribution of the forces of compression and tension in a medial-to-lateral direction, or additional forces of bending and torsion. From a clinical perspective the force of compression may be dominant to other forces in determining a horse’s response to circling, but it is not the only factor. Extension of the limb is also influential.5 When the lesion is in the outside limb while the horse is circling and undergoing compression, exacerbation of the lameness occurs. For instance, lameness in horses with medially located lesions of the distal phalanx or of the third carpal bone is worse when the limb is on the outside of the circle and the lesion is being compressed. For some soft tissue injuries, tension forces may be more important. Lameness in horses with proximal suspensory desmitis often is worse with the limb on the outside of the circle, suggesting that tension is important in the expression of lameness. The same observation is not seen in horses with more distally located suspensory desmitis. Is the lameness seen in a horse that is moving in a circle the same lameness that is seen while the horse is walking or

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trotting in straight lines? In most instances, circling exacerbates the primary lameness seen in straight lines. If lameness is subtle or nonexistent when the horse is evaluated in a straight line, the lameness seen during circling becomes the baseline lameness. The clinician must recreate the same conditions of circling when evaluating the results of diagnostic analgesic techniques. There is always the possibility that lameness seen during circling may be different from the baseline lameness seen in straight lines. For example, a horse has grade 1 RF baseline lameness when it moves in a straight line that increases to grade 3 when trotted in a circle to the left, but still has grade 1 lameness when trotted to the right. Lameness in a straight line and when trotting to the right is absent after palmar digital analgesia but still is rated grade 3 when the limb is on the outside of the circle. This horse has two problems in the RF: palmar foot pain and an additional carpal lameness that becomes evident when the horse is trotted to the left (RF on the outside of the circle). With bilateral forelimb or hindlimb lameness, primary lameness often is seen in a single limb in straight lines, but during circling the lameness is seen in whichever limb is on the inside (or outside) of the circle. Circling is useful in exacerbating the primary lameness problem and identifying an additional cause of lameness not previously noted. This additional lameness must be recognized and treated separately from the baseline lameness. Good correlation usually exists between the cause of lameness seen on the straight and that seen while circling the horse; thus it is helpful to circle the horse to try to exacerbate lameness. Circling can be done at the walk and trot in hand and while lunging or riding the horse. Horses often move more freely and naturally when lunged than when being led.5 However, lunging is not possible in some horses, particularly racehorses, and circling while being led is better than no circling. The surface should be nonslip because horses may be hesitant to move freely on slippery surfaces and shorten or alter the stride even when lameness is not present.5 Soft footing is best when the horse is first being lunged, because the horse can buck and play without risk of injury. Hard or firm surfaces are best to exacerbate many lameness conditions, but the surface must be nonslip to avoid possible injury. That lameness of the upper forelimb or hindlimb is worse when the limb is on the outside of the circle is a common misconception. This is true in some horses, but a generalization cannot be made (see following text). Shortening of the cranial phase of the stride may appear more obvious with the limb on the outside of the circle, but exacerbation of lameness judged by the degree of head nod may not be observed. Another misconception is that horses with lameness of the foot are lamest when the limb is on the inside of the circle. Although a majority (65%) of those with lameness localized to the foot are lamest when the limb is on the inside of a circle, lameness can be worst with the lame limb on the outside of a circle. This depends in part on the location of pain within the foot.

Forelimb

Lameness Worsened with Limb on the Inside of the Circle

In many horses, lameness originating from the fetlock region to the foot is worse with the affected limb on the inside of the circle. Comparison of circling on hard and soft surfaces is useful. Baseline lameness associated with

foot pain usually is dramatically increased when the horse is circling on a hard surface, but a less obvious response is seen when circling on softer surfaces. However, lameness in horses with medially located lesions can be worse with the limb on the outside of the circle. Horses with lameness of the metacarpal region vary in response to circling. Lameness related to metacarpal bony injury and distally located lesions in the suspensory ligament or digital flexor tendons tends to be worse with the limb on the inside of the circle, whereas lameness in those with proximal suspensory desmitis is worse with the limb on the outside. Horses with suspensory branch desmitis may show a different response depending on lesion severity and whether the injured branch is undergoing tension or compression. In my experience, the degree of lameness in horses with pain originating from the forearm, elbow joint, arm, and shoulder joint region tends to be worse with the limb on the inside of the circle, but opinions and experiences do vary.5 Observations may differ if horses are examined while led in hand as opposed to being lunged or ridden. Lameness in some horses with mechanical restriction of movement that dramatically decreases the cranial phase of the stride may be worse with the limb on the outside of the circle.

Lameness Worsened with Limb on the Outside of the Circle Horses with medially located lesions of the lower limb, especially foot lameness, proximal metacarpal lesions (proximal suspensory desmitis or avulsion injury to the McIII at the suspensory origin), or carpal pain often are more lame with the limb on the outside of the circle. Horses with lesions in the antebrachiocarpal joint are less consistent in response to circling compared with those with middle carpal joint lesions, because most of the common injuries involve the medial aspect of the latter. Upper limb lameness is accentuated in some horses.5

Lameness Improved When Circling

Lameness that appears better on a circle than in straight lines is uncommon. Lameness in horses with medially located lesions in the foot or carpus may improve when the limb is on the inside of a circle. Baseline lameness in horses with middle carpal disease involving the third and radial carpal bones improves with the limb on the inside of the circle. A STB racehorse with grade 2 or 3 RF baseline lameness in a straight line that increases to grade 3 or 4 when circled to the left, but is only grade 1 or 2 when circled to the right, may have lameness associated with the middle carpal joint, but pain in the medial aspect of the foot also is possible. A horse with bilateral forelimb lameness (e.g., a horse with grade 3 RF baseline lameness in straight lines) may show grade 3 to 4 RF lameness when trotting to the right but grade 1 LF lameness when trotting to the left. The primary lameness is in the RF, and lameness is worse when the limb is on the inside of the circle. Circling to the left induced lameness in the LF, masking the RF lameness, because bilateral lameness existed that was not recognized when the horse was trotting in a straight line.

Hindlimb Lameness and Circling

In my experience, baseline lameness in most horses with any hindlimb lameness is worse when the limb is on the

inside of the circle. Exceptions do exist, and some have different experiences and thus opinions.5 Lameness associated with proximal suspensory desmitis often is worse with the affected limb on the outside of the circle, and the horse may stumble or take bad steps. Lameness in some horses with stifle lameness appears worse with the affected limb on the outside of a circle, but in others it appears similar to the left and the right. Many conditions of the stifle involve the medial femorotibial joint, a location that would be compressed with the limb on the outside. Lameness in any horse with a medially located lesion involving the distal hindlimb could be worse with the limb on the outside of the circle. Circling may be useful in exacerbating a primary lameness but generally is not helpful in localizing pain causing lameness.

Observation during Riding

Lameness may not be apparent when the horse is evaluated in hand in straight lines and circles but is obvious when the horse is ridden. This lameness becomes the baseline lameness for further investigation. The additional weight of a rider can exacerbate both forelimb and hindlimb lameness. Gait abnormalities and performance in horses with primary back pain or those with substantial muscle pain secondary to hindlimb lameness usually are worse when they are ridden. Hindlimb gait restriction can occur in horses with back pain but may be apparent only when a horse is ridden.5 Problems related to an ill-fitting saddle or girth, behavioral problems, head shaking, abnormal posture or carriage of the head and neck, and refusal to take a lead or bend in certain directions may be evident only when a horse is ridden. A horse may be easier to control when ridden than when in hand or on the lunge. Performance of specific maneuvers by the horse may accentuate lameness. A collected trot that forces more weight onto the hindlimbs may exacerbate hindlimb lameness. An extended trot may reveal the horse’s inability to extend one limb compared with another and reveal lameness that was completely imperceptible under all other circumstances. The primary complaint, such as poor-quality flying changes of lead at canter, may require a riding assessment regardless of whether baseline lameness is evident under other circumstances. However, it is important for the veterinarian to separate his or her observations from those perceived by the rider. Identification of the lame limb may be difficult for a rider, although he or she may have a very strong opinion. If the veterinarian’s observations differ, the rider may be difficult to convince. It is also essential to recognize that bad riding can actually induce a false lameness that is completely unapparent if the horse is ridden well. Nonetheless, an experienced rider, trainer, or driver can be quite helpful in assessing the horse’s response to diagnostic analgesia or therapy, particularly in horses with thoracolumbar pain, subtle hindlimb lameness manifested only when ridden, and poor performance related to a musculoskeletal problem. Working regularly with a skilled, experienced, and reliable rider can be very helpful. Subtle differences in weight distribution of the rider may exacerbate or mask the presence of forelimb and especially hindlimb lameness. When the horse is performing the posting (rising) trot, lameness may be more or less

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prominent depending on which diagonal the rider is using. In the rising trot the rider sits on either the left or right diagonal. On the left diagonal the rider is sitting when the LF and RH are bearing weight and rising during the swing phase of these limbs. On the right diagonal the rider is sitting when the RF and LH are bearing weight. The correct diagonal is the outside diagonal (i.e., left diagonal on the right [clockwise] rein). Hindlimb lameness often is worse when the rider sits on the diagonal of the lame limb.5 Therefore if the horse is lame in the RH, the lameness appears and feels worse when the rider sits on the left diagonal. Horses with hindlimb lameness may try to force or throw the rider to sit on the more comfortable (for both horse and rider) diagonal.5 A horse with bilateral hindlimb lameness may appear lame in the RH when the rider sits on the left diagonal and lame in the LH when the rider sits on the right diagonal.5 Forelimb lameness is influenced less by the diagonal on which the rider sits, but a similar pattern exists. RF lameness is worse with the rider sitting on the right diagonal.5 This difference in lameness expression may be perceptible only by an experienced rider. Mild hindlimb lameness may become most obvious when a horse is ridden in small figure eights (two 10-m–diameter circles linked), especially when the horse changes direction from left to right or from right to left.

Observation of Inclines

Walking or trotting a horse uphill or downhill may exacerbate lameness or identify previously unapparent lameness. Lameness in horses with suspensory desmitis may be worse when they walk uphill or downhill. Lameness associated with palmar foot pain may be worse when the horse walks downhill, and the horse may show a tendency to stumble. Horses that tend to stumble or knuckle behind while walking downhill may have loose stifles (inability to maintain the position of the patella, usually caused by lack of muscle tone). Horses with neurological disease usually show more pronounced clinical signs when walking uphill or downhill. A superficially flat, hard surface may actually slope; this can influence lameness because the horse’s feet will be tilted with one side lower than the other. Thus the horse may appear different when trotting away from the observer than when returning.

EVALUATION OF LAMENESS WITH A TREADMILL OR GAIT ANALYSIS The use of a treadmill for poor performance evaluation is well recognized, and its use in lameness assessment is discussed in detail in Chapter 98. The clinical relevance of lameness apparent only on a treadmill is open to debate. I do not find lameness examinations on a treadmill at high speed particularly useful unless slow-motion videotape is available. I prefer to assess the horse while training or performing. A horse may modify its normal gait on a treadmill. Good correlation was demonstrated between gait regularity in horses exercised on a track and a treadmill, but treadmill strides and steps were shorter, and the swing phase of the stride was reduced.34 Horses require at least

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two training sessions on a treadmill before the gait becomes consistent.35 Stride characteristics of horses galloping on a treadmill change as the slope of the treadmill increases from 0% to 8%; horses reduced the suspension phase to maintain overall stride length.36

Gait analysis is discussed in Chapter 22. To date in the clinical setting, assessment by an experienced, skilled observer has been more reliable in the identification of the lame limb or limbs than other, more sophisticated methods of gait analysis.

Chapter

8 

Manipulation Mike W. Ross Flexion or other manipulative tests often are used to induce or exacerbate lameness during lameness or prepurchase examinations.

INDUCED AND BASELINE LAMENESS It is important to understand the concept of induced lameness and the possible difference between lameness seen at this stage and baseline lameness. During lameness examination, baseline lameness is established before any form of manipulation is performed. This may be difficult if more than one limb is involved, if lameness is subtle or subclinical, or if lameness is bilaterally symmetrical, which causes a gait abnormality without overt lameness. Lameness provocation is performed to exacerbate the baseline lameness or to provoke a hidden gait abnormality and attempt to localize the source of pain within a limb or limbs. Provocative tests create induced lameness that may not have any clinical relevance to the baseline lameness observed during initial movement. These tests are not sensitive or specific and often result in false-positive and falsenegative findings. Many horses with palmar foot pain respond positively to the “fetlock flexion test” (or lower limb flexion test, see following text) and could erroneously be thought to have lameness of the metacarpophalangeal joint. Similarly, a horse with proximal suspensory desmitis (PSD) may show exacerbation of lameness after distal limb flexion. A racehorse with baseline lameness as the result of a carpal chip fracture may have preexisting low-grade osteoarthritis of the metacarpophalangeal joint and respond positively to lower limb flexion but response to carpal flexion may be equivocal. Diagnostic analgesia is essential to localize the source or sources of pain. In the hindlimb, hock flexion, the so-called “spavin test,” causes many false-positive reactions.

FLEXION TESTS

References on page 1257

Flexion tests were first described early in the twentieth century, but information regarding the degree of flexion, force, or duration of the tests was lacking.1 Variations in technique persist and produce variable responses that can be misleading. There appear to be more false-positive reactions to flexion than there are false negatives, but the

latter do occur. Flexion tests are useful during prepurchase examinations because the horses being examined usually are relatively sound, and the tests are useful at uncovering hidden sources of pain. Flexion tests may be useful in exacerbating lameness, particularly when the primary or baseline lameness is in the region being flexed, but sensitivity is doubtful. Horses judged to be clinically sound underwent a “normal” and then a “firm” lower limb flexion test (fetlock flexion).2 Of the 50 horses tested, 20 had a positive response to normal flexion, and 10 of these horses were judged to be lame while trotting for about 15 m (50 feet) or more. Forty-nine of 50 horses had a positive response to firm flexion, and 35 of these remained lame for a minimum of 15 m. In this study the force applied was not calibrated, 7 of the 50 horses developed lameness within 60 days of completion of the study, and 24 horses had radiological abnormalities that could have contributed to a positive response to flexion.2 Although there may be an explanation for a positive response in some horses, the high percentage of positive results in the study is in agreement with my clinical impression. In a study using the Flextest (Krypton Electronic Engineering NV, Leuven, Belgium), an apparatus designed to control traction force and time during a lower limb flexion test, the optimal force and time for flexion were 100 N and 1 minute, respectively. There was a positive response to flexion in many horses that were considered sound, and a positive response in sound horses was more likely in those in active work than in horses that had been rested or turned out on pasture. Horses were more likely to manifest a positive response to flexion as the force used in the test was increased.3 A false-positive response to flexion can be observed in clinically normal horses and in those with unimportant low-grade problems. Lameness induced by flexion in these horses may have little clinical relevance. However, other evidence suggests that a positive response to lower limb flexion in sound horses may be useful to predict future lameness. In a retrospective study, 151 initially sound horses were followed for 6 months. Twenty-one percent of horses with a positive forelimb flexion test result developed lameness in the area being flexed, whereas only 5% of horses with a negative flexion test result subsequently developed lameness. In young Swedish Warmbloods there was a positive correlation between a positive response to flexion and a subsequent insurance claim related to lameness.4 In a more recent study the predictive value of the lower limb flexion test was debated.5 Sixty percent of sound horses responded positively to the flexion test. There was no influence of body weight, height, or range of motion, but outcome of the flexion test increased significantly with age and in mares. Over a 6-month period the number of horses responding positively decreased significantly, a

finding that casts doubt on the possible predictive value of the test.5 Flexion tests lack specificity because it is nearly impossible to flex a single joint without flexing other joints or nearby tissues, particularly in any hindlimb or distal forelimb flexion tests. Elevation of a limb without flexion in severely lame horses may exacerbate the baseline lameness, because horses guard the limb or need to warm out of the lameness for a number of steps while trotting, thus complicating interpretation. Hindlimb flexion tests are less specific than forelimb tests because the reciprocal apparatus prevents flexion of any joint without concomitant flexion of other joints. Hindlimb flexion tests are useful in exacerbating baseline lameness, but positive responses to individual lower limb and upper limb tests, in my opinion, only localize pain causing lameness to the entire hindlimb. I believe that flexion tests are useful in exacerbating lameness, and in some horses it is the baseline or relevant lameness that is being worsened. In general, unless the horse’s response is clearly pronounced and different from that of other manipulation, lameness cannot be localized based on response to flexion alone. Diagnostic analgesia should always be used, when possible, to localize pain.

Order, Duration, Force, and Venue during Flexion Tests

Consistency in technique is essential. Although force exerted by individuals varies, the flexion technique of experienced practitioners is sufficient to objectively assess response to flexion.6 Response to flexion can and should be compared with response in the contralateral limb. Ideally the flexion test should be performed in the contralateral sound limb first before being performed in the suspect limb, to determine the horse’s response. Accurate assessment of response to flexion in the contralateral nonlame limb may not be possible if the horse is severely lame after flexion of the lame limb and lameness persists. In some instances, baseline lameness is actually increased by forcing the horse to stand for the contralateral flexion test, a useful observation seen most commonly in horses with forelimb lameness (see following text). Horses with nearly bilaterally symmetrical lameness may have a similar positive test result in the less-lame contralateral limb. Duration of flexion is somewhat controversial and may be an individual choice. In a study evaluating lower limb flexion, duration of 1 minute was considered ideal, because normal horses that underwent flexion at 100 N for 1 minute had few false-positive responses.3 Maintaining firm flexion for 1 minute while performing all flexion tests and repeating the tests in the contralateral limbs can make this portion of the lameness examination time-consuming. On the other hand, if the clinician takes the time to perform these tests, optimum chances of success are improved. A false-positive result is more useful than a false-negative test result. Some clinicians prefer to perform flexion tests with more force but for a shorter duration. This technique works well for lower limb flexion tests. Seldom is it possible to maintain some upper limb manipulative procedures for 1 minute. Thus some latitude is necessary. I believe that duration of flexion of 45 seconds to 1 minute is enough to elicit an accurate response in most horses. Force used during flexion varies considerably, but excessive force induces lameness in most normal horses.

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Forces in the range of 100 to 150 N represent a moderate degree of force for lower limb flexion tests. In studies using a dynamometer, the maximum amount of force that could be used without a consistent withdrawal response in normal horses was 150 N.7 The amount of force also depends on the size of the horse or the joint being flexed. The amount of force used in adult horses cannot be used in foals. Horses with obvious osteoarthritis or articular fracture, or those with substantial soft tissue injury likely to be affected by the flexion test, do not tolerate the same force as horses with more mild conditions. In a study of healthy and injured Thoroughbred (TB) racehorses, a positive correlation existed between decreased range of motion and joint injury.8 Loss of joint motion was most likely caused by joint capsule fibrosis, but pain associated with increased intraarticular pressure from effusion or flexion also may have limited joint motion.8 I recommend flexing a joint as much as possible with an amount of force just slightly less than the force that consistently causes a withdrawal response. Consistency should be applied between horses, paying attention to how the horse reacts; obvious resistance to sustained passive flexion may be clinically significant. Proper evaluation of the results of flexion tests requires that the horse be observed while trotting in a straight line on a firm, nonslip surface. Evaluation during trotting is important to differentiate those horses resistant to static flexion from those with an authentic positive flexion test result. Horses usually are trotted in hand, although occasionally a horse’s response to flexion is evaluated while it is being ridden. The horse should be trotted immediately after the limb is placed to the ground, with care taken to avoid scaring the horse or providing any excessive encouragement to trot, because many horses will slip initially, gallop off, or balk, all of which necessitate test repetition. If possible, the horse should be trotted away from the examiner for a minimum of 12 to 15 m.

Causes of Pain during Flexion and Positive Flexion Test Results

Forced flexion of a joint can induce pain in many potential sites. Force is being applied to both articular structures and surrounding soft tissues. The tissues on the flexion side of the joint are being compressed, whereas tissues on the extension side are under tension. During flexion, intraarticular pressure and intraosseous pressure in subchondral bone are increased.3,8 Stretching or compression of the joint capsule, vascular constriction, and activation of pain receptors in the joints and surrounding soft tissues also can occur during flexion.3 It is rarely possible to attribute pain on static flexion or during movement after flexion to an individual articular surface. The “fetlock flexion test” is a misnomer because as it is commonly performed it includes the interphalangeal joints and stresses surrounding soft tissue. Thus the names lower limb flexion test or fetlock region flexion test are more appropriate.

Positive Responses to Flexion

Positive responses to flexion can be seen with static flexion (see Chapter 6) and when movement follows flexion. A positive flexion test result is defined as obvious lameness or an increase over baseline lameness that is observed for more than three to five strides while the horse trots in a straight line after flexion. A mild response, even in sound

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horses, often is seen in the first few strides, a finding that should be compared with the contralateral limb. Sound horses warm out of this mild response quickly. Of 100 sound horses 50% had a slight response, 35% had mild lameness and 15% had distinct lameness after a lower limb flexion test.5 A persistent, one- to two-grade increase over baseline lameness for several steps is a positive response. In horses with hindlimb lameness a marked positive response often is accompanied by reluctance to place the heel on the ground, and the horse may land only on the toe for several strides.

Forelimb Flexion Tests Lower Limb Flexion Test

The lower limb flexion test often has been equated erroneously with the fetlock flexion test. The fetlock region can be flexed independently of interphalangeal joints (see following text). The lower limb flexion test is the most common test performed in the forelimb and involves placing a hand on the toe and forcing the fetlock and both interphalangeal joints into firm flexion (Figure 8-1). A positive response to flexion can be observed with any condition of the distal interphalangeal, proximal interphalangeal, and metacarpophalangeal joints or the navicular bone or bursa; other causes of palmar foot pain; digital flexor tenosynovitis; any soft tissue problem in the palmar pastern region; and lameness associated with the branches or proximal aspect of the suspensory ligament (SL) or proximal sesamoid bones (PSBs). Horses with lesions of the PSBs usually have markedly positive responses to this test. This test is not specific for lameness of the metacarpophalangeal joint. I have seen marked responses in horses with navicular disease or osteoarthritis of the interphalangeal joints. However, horses with osteoarthritis, fractures of the metacarpophalangeal joint, or tenosynovitis usually also show

Fig. 8-1  •  The lower limb flexion test is often erroneously called the fetlock flexion test. During the lower limb flexion test the fetlock, proximal interphalangeal, and distal interphalangeal joints are flexed; the palmar pastern and fetlock region soft tissue structures are compressed; and the dorsal structures are stretched.

a marked positive response. In a recent study of clinically sound horses in which lameness could consistently be induced by flexion with 250 N for 1 minute, lameness was alleviated by intraarticular analgesia of the metacarpophalangeal joint, but not by intraarticular analgesia of the proximal interphalangeal or distal interphalangeal joints or intrathecal analgesia of the navicular bursa.9 Exacerbation of lameness associated with pain arising from the SL after lower limb flexion is probably caused by relaxation of the SL during flexion and then sudden loading of the ligament when the horse starts to load the limb. The limb should be held as close to the ground as possible, and forced carpal flexion should be avoided (see Figure 8-1). All soft tissue and bony structures in the palmar aspect of the distal limb are severely compressed, resulting in low specificity for the metacarpophalangeal joint. Some people use a hand as a fulcrum or grab the toe with both hands (Figure 8-2), but this technique may result in application of excessive force, although it otherwise produces similar results.

Fetlock Flexion Test

The specificity of the lower limb flexion test can be improved by applying force to the metacarpophalangeal joint and avoiding forced flexion of the interphalangeal joints. The fetlock flexion test is performed by placing one hand along the dorsal aspect of the pastern region and one hand along the dorsal aspect of the metacarpal region, while avoiding flexion of the carpus (Figure 8-3). When compared with lower limb flexion this test is more difficult to perform because it requires more force and the clinician’s effort to maintain a similar degree of flexion. The test is not specific

Fig. 8-2  •  Extreme lower limb flexion can be achieved by using both hands on the toe with the limb cradled between the clinician’s legs. With such extreme flexion even normal horses may manifest a positive response.



Fig. 8-3  •  A true fetlock flexion test can be performed by carefully flexing only the fetlock joint. The clinician’s hand grasps only the pastern and not the toe of the hoof while avoiding forced flexion of the proximal and distal interphalangeal joints (see Figure 8-1).

for articular lameness of the metacarpophalangeal joint, and horses with soft tissue problems respond positively.

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Fig. 8-4  •  The carpal flexion test is the most specific of all flexion tests, but it applies concomitant mild flexion of the elbow and shoulder joints. Although false-negative results are possible, a positive carpal flexion test result usually means that lameness originates from the carpal region.

Flexion of Interphalangeal Joints

In my opinion, flexion of either the proximal interphalangeal or distal interphalangeal joint without concomitant flexion of the other, or of the metacarpophalangeal joint, is impossible. Varus or valgus stress can be applied to the interphalangeal joints, and when followed by trotting, this stress can be a suitable provocative test in horses with osteoarthritis or soft tissue injuries of these joints.

Carpal Flexion Test

The carpal flexion test is the most specific of all forelimb flexion tests, and a positive response usually reflects baseline lameness associated with the carpal region. Few falsepositive results occur. A positive response may reflect intraarticular pain, but a positive response also is seen in horses with carpal tenosynovitis, accessory carpal bone fractures, proximally located superficial digital flexor (SDF) and deep digital flexor (DDF) tendonitis, PSD, or avulsion fracture of the third metacarpal bone (McIII) at the SL origin. Rarely, a horse with a problem in the scapulohumeral and cubital joints or the antebrachium responds positively. A negative response does not preclude an articular lesion of the carpus, including incomplete fractures or sclerosis of the carpal bones. The limb is elevated, and the carpus is forced into full flexion by pushing the metacarpal region directly underneath the radius (Figure 8-4). The distal limb can be pulled laterally to place the carpal joints in valgus stress or torsion. Horses sometimes trot off lame on the contralateral limb after the carpal flexion test is performed. I have seen this most commonly in young Standardbred or TB racehorses with subchondral bone pain in the middle carpal joint and call it the “Ross crossed-extensor phenomenon.” I believe that this reflects bilateral lameness, and flexion of the ipsilateral carpus causes less pain than making the horse stand for 1 minute on the contralateral limb. I have observed this response most commonly in horses with bilateral carpal lameness, but exacerbation of contralateral

Fig. 8-5  •  Upper forelimb flexion is performed by grasping the antebrachium and pulling the entire limb caudally and slightly proximally. This maneuver flexes the shoulder joint and extends the elbow joint. Horses with shoulder region lameness often respond positively to this manipulative test.

lameness is not restricted to carpal lesions. Dyson10 has called this a “paradoxical response to flexion” and has observed exacerbation of contralateral lameness in horses with navicular syndrome, DDF tendon lesions in the digit, and distal hock joint pain.

Upper Limb Manipulation

Because of the inverse but simultaneous movement of the elbow and shoulder joints, it is difficult to accurately name the flexion tests of these joints. For instance, when the limb is pulled in a caudal direction, the shoulder joint is flexed but the elbow joint is extended. I call this manipulation upper limb flexion (Figure 8-5). This maneuver requires both

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Fig. 8-6  •  The upper limb extension test is performed by pulling the forelimb out in front of the horse and forcing it proximally. This places the elbow joint in flexion and the shoulder joint in extension. In my experience, lameness of the elbow region is exacerbated by this technique, but occasionally shoulder joint lameness also is worsened.

hands, one hand grasping the pastern region and one grasping the cranial aspect of the antebrachium to force the entire limb in a caudal direction. When the limb is pulled in a cranial direction, resulting in upper limb extension, the shoulder joint is extended, but the elbow joint is flexed (Figure 8-6). Both hands are placed around the pastern region while forcing the entire forelimb into maximal extension. Maintenance of upper limb extension or flexion for even 45 seconds is difficult, so I try to maintain this position for as long as possible and then evaluate the horse while trotting. Many normal horses resist upper limb manipulation, and an alternative is to force the limb into hard flexion or extension in a rhythmical fashion six to eight times and then trot the horse. Even though the entire limb is being manipulated, there are few false-positive test results. A horse with a positive response to carpal flexion may have a similar response to upper limb manipulation because it is difficult to perform upper limb flexion without simultaneously flexing the carpus. False-negative test results can occur, probably because of the inability to place either the shoulder or the elbow joints in hard flexion. In my experience, horses with lameness originating from the elbow region are more likely to respond to upper limb extension, whereas those with lameness originating from the shoulder region are more likely to respond to upper limb flexion.

Hindlimb Flexion Tests

Hindlimb flexion tests are not specific, but they may be useful to exacerbate the baseline lameness or detect hidden sources of potential lameness. I do not believe that hindlimb flexion tests are useful in differentiating the source of pain causing lameness in most horses unless the response is dramatic, and diagnostic analgesia usually is required in all horses.

Fig. 8-7  •  The lower limb flexion test in the hindlimb is performed with the limb as close to the ground as possible. Flexion of one portion of the hindlimb is impossible without flexing the entire limb, a finding that explains many false-positive hindlimb flexion test results.

Lower Limb Flexion Test

The lower limb flexion test is performed similarly to the forelimb flexion test, but with similar force the metatarsophalangeal joint can be flexed more extremely. The veterinarian should try to keep the limb as low as possible to avoid placing hard flexion on the upper limb, although all joints are flexed to a degree. The lower limb flexion test also affects the proximal interphalangeal and distal interphalangeal joints and the surrounding soft tissues (Figure 8-7). Horses with digital flexor tenosynovitis or DDF tendonitis show a marked response to the lower limb flexion test. False-positive results can occur, but these are less common in a hindlimb than in a forelimb, even in horses in active work. Horses with pain in the upper limb may show a mild or moderate response to lower limb flexion. This test is not specific for pain located in the lower limb, and lameness in horses with stifle pain often is worse after the lower limb flexion test.10 Horses with subchondral bone pain from maladaptive or nonadaptive bone remodeling of the distal aspect of the third metatarsal bone (MtIII) or those with incomplete fractures of the MtIII or incomplete midsagittal fractures of the proximal phalanx may show little response to this test (false-negative result). Coupled with lack of effusion of the metatarsophalangeal joint, a false-negative response to lower limb flexion may sidetrack the clinician into thinking pain originates elsewhere. Diagnostic analgesia is required to determine the source of pain.

Fetlock Flexion and Interphalangeal Joint Tests

The metatarsophalangeal joint region can be flexed independently of the interphalangeal joints in the hindlimb, or the interphalangeal joints can be flexed independently, but these tests are difficult to perform and of limited value.

Upper Limb Flexion Test

The so-called “spavin test” or “hock flexion test,” misnomers for the upper limb flexion test, is not specific for



Fig. 8-8  •  The hindlimb upper limb flexion test is demonstrated. This test has been called the spavin test or hock flexion test, but it is not specific for lameness of the hock. The hock and stifle joints are in forced flexion, the lower limb joints are flexed, the metatarsal region is compressed, and a small amount of forced flexion of the coxofemoral joint is induced.

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Fig. 8-9  •  A hindlimb flexion test is a combination of the lower limb flexion and upper limb flexion tests.

lameness of the hock because the stifle and coxofemoral joints also are stressed hard, and mild flexion of the lower joints is inevitable. The terms spavin test and hock flexion test are deep-rooted in our profession but it is important to recognize that a positive response is not synonymous with distal hock joint pain. The limb is held in hard flexion for at least 1 minute, but additional time for this test may improve its clinical value (Figure 8-8). It may be necessary to have an assistant place a hand on the contralateral hip to steady the horse, because proper performance of this test requires that the limb be elevated substantially, and the horse may lose its balance. The position of the hands in the metatarsal region is important to consider, because the force required to hold the hindlimb in this position may cause compression and pain in structures along the plantar aspect, potentially contributing to a false-positive response.

Hindlimb Flexion Test

Alternatively, the entire hindlimb can be flexed simultaneously. This test is useless in differentiating potential sources of pain in a limb, but it is quite useful in exacerbating baseline lameness or uncovering occult lameness conditions. The clinician’s hands are placed on the toe and the entire limb is held in extreme flexion (Figure 8-9). An assistant may be necessary to steady the opposite hip while the limb is elevated.

“Hock” Extension Test

Hock extension may be useful in placing selective stress on the hock, independent of the stifle. Forced extension causes tension on the soft tissue structures on the dorsal, medial,

Fig. 8-10  •  During the hock extension test the clinician forces the hock into extension by pushing down on the calcaneus while pulling up on the distal limb by using both the right arm and left leg. Pain from hock lameness can be exacerbated, but false-positive results from pain in other locations also can occur.

and lateral aspects of the hock. Seldom is it possible to perform this test for 1 minute; six to eight attempts at forced extension followed by trotting the horse can be substituted for more lengthy manipulation (Figure 8-10). False-positive and false-negative responses occur, which are caused mostly by the inelastic reciprocal apparatus. This

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Fig. 8-11  •  A seldom-used test is the stifle flexion test. This test can be difficult and dangerous to perform in fractious horses. The forced flexion of the stifle joint used in this test attempts to differentiate stifle and hock joint pain.

maneuver can reveal laxity of a damaged fibularis (peroneus) tertius.

“Stifle Flexion” Test

A modification of the upper limb flexion test can be used to place hard flexion on the stifle, independent of the hock (Figure 8-11). This test can be somewhat difficult to perform but may exacerbate lameness in horses with osteoarthritis or other conditions of the stifle. Other proximal limb joints are also in flexion; therefore some false-positive results occur. See page 87 for other manipulation of the stifle.

DIRECT OR LOCAL PALPATION FOLLOWED BY MOVEMENT Static palpation, in which the horse’s response to compression during palpation while standing is assessed, reveals useful information (see Chapter 6). Additional information can be gained by evaluating movement after palpation and dynamic provocation to induce lameness. Dynamic provocation usually is performed by digital palpation or use of hoof testers. Many horses manifest a positive response during static palpation, but the primary pain is located elsewhere. However, if lameness can be induced or baseline lameness can be increased by one or two grades by deep palpation, then the area may be relevant to the current cause of lameness. False-positive results do occur, but in my opinion these are less frequent than with most flexion tests. There are few false-negative results.

Digital Compression of a Painful Area

The veterinarian should elevate the limb and compress the painful or otherwise inflamed area for 15 to 30 seconds and then evaluate the horse at a trot in hand. Exacerbation of the baseline lameness by one or more grades is considered

a positive response. This procedure is useful in differentiating the cause of lameness in both the forelimb and hindlimb. In the forelimb, I find it useful to compress the dorsal proximal aspect of the proximal phalanx (if a midsagittal fracture is suspected), the dorsal cortex of the McIII (for bucked shins or a dorsal cortical fracture), exostoses involving the small metacarpal bones (for splints), the suspensory branches or digital flexor tendons, and the proximal palmar metacarpal region (for PSD or longitudinal or avulsion fracture of the McIII). In horses with mild SDF tendonitis, baseline lameness usually is mild or nonexistent, but obvious lameness after digital compression suggests tendonitis as a clinically significant problem. In the hindlimbs, compression of the dorsal proximal aspect of the proximal phalanx can increase lameness from midsagittal or dorsal frontal fracture, but trauma from interference injury (of particular importance in trotters) or other forms can lead to a false-positive response. A dynamic Churchill test, compression followed by trotting (see Chapter 6), is useful in the diagnosis of lameness of the proximal metatarsal region and tarsus. In the hindlimb, compression of the proximal aspects of both the second and fourth metatarsal bones puts indirect pressure on the origin of the SL, and a positive response may indicate PSD. False-positive results to this provocative test are common because the entire hindlimb is in flexion, similar to upper limb flexion without compression. Compression of a “curb” followed by trotting may increase lameness. In some horses with tibial stress fractures, an induced lameness can be seen after deep palpation of the caudal tibial cortex. With the limb elevated, the veterinarian should apply deep pressure to the caudal cortex by wrapping the fingers around the tibia from the medial aspect (see Figure 6-27). Most horses object to this maneuver, but in those with tibial stress fractures, the positive static response is followed by an exacerbation of the baseline lameness.

Axial Skeleton

Application of direct local pressure to many parts of the axial skeleton is difficult, but in some instances this procedure can lead to the detection of pain both statically and while the horse is trotting (see Chapters 6, 93, 95, and 97). In the cervical area, forced lateral bending followed by walking or trotting may exacerbate neurological signs or gait deficits in horses with cervical instability or proliferative changes. Deep palpation over the thoracolumbar spine followed by trotting can induce hindlimb stiffness or other mild gait abnormalities. Direct and deep palpation over the tubera sacrale and tubera coxae can induce hindlimb lameness in horses with stress fractures or those with chronic lameness as a result of pelvic asymmetry from old fractures. Sacroiliac compression, or manipulation of the sacrum or tail head, can induce hindlimb stiffness or lameness in horses with injuries in these areas.

INDUCED LAMENESS AFTER HOOF TESTER EXAMINATION The hoof testers are applied in a suspected area for 15 to 30 seconds and the horse is evaluated for lameness while trotting. False-positive test results are quite common, but



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a marked difference between limbs can be an important clinical sign. Shoes and pad combinations may preclude complete hoof tester examination of the sole, so I often apply pressure across the heel. I have found this position to yield the most useful information in horses with palmar foot pain from most causes, but it also induces a positive response in horses with nonspecific foot pain (sore feet). Most normal horses object to firm pressure placed across the heel using hoof testers, particularly in a hindlimb, and mild lameness on the initial few steps is common, but severe lameness after this test is a useful indication that the foot is the source of baseline lameness.

THE WEDGE TEST The wedge test is a form of manipulation similar to the flexion or other varus or valgus stress tests, but it is used specifically to evaluate the digit and associated soft tissues. The wedge can be used to dramatically change the dorsalto-palmar (heel) or medial-to-lateral hoof angles. Collateral ligaments, joint capsules, subchondral bone and articular surfaces, and surrounding soft tissues can be stretched or compressed when the horse stands on the wedge. Changes in hoof angles of this magnitude can greatly change the stress placed on the DDF tendon, SDF tendon, and SL. Raising the heel reduces stress on the DDF tendon but increases stress on the SL. Raising the toe reduces stress on the SL but increases stress on the DDF tendon, navicular bone, and associated ligaments and bursa. The number of tissues affected by the wedge accounts for the lack of specificity of this test, and it likely accounts for many falsepositive results. The wedge is placed in the desired position, and the horse is made to stand in this position for 30 to 60 seconds with the contralateral limb elevated (Figure 8-12). The horse is then trotted in a straight line on a firm surface. The test can be used in any limb but is performed most commonly in the forelimbs. In some horses, it is difficult to attain the desired duration regardless of whether they are lame. The horse’s response to simply standing on the wedge may not give an accurate indication of how lame it will be when it is trotted. In horses content to stand in such an abnormal position, a dramatic lameness may be seen at the trot. Horses with navicular syndrome or sore feet from many causes of palmar foot pain are most likely to manifest a positive response. In my experience and that of others, the direction of the wedge that elicits the most positive response from horses with palmar foot pain is with the apex (low end) directed medially (see Figure 8-12).11 This substantial change in the medial-tolateral hoof angle is likely to cause stretching of the suspensory apparatus of the navicular bone and collateral ligaments of the distal interphalangeal joint or compression on articular structures. Horses with palmar foot pain may show severe lameness, but diagnostic analgesia is required to confirm the foot as a source of pain. Horses with injuries of the DDF tendon, SDF tendon, and SL may show a milder response.

VARUS OR VALGUS STRESS TESTS Evaluation for lameness after placing varus or valgus stress on an individual joint may incriminate this area as a potential source of pain and is used most commonly in the stifle.

Fig. 8-12  •  A 15- to 20-degree wedge can be used to manipulate the joints and soft tissue structures of the digit. The most consistent response is elicited by directing the apex (low end) of the wedge medially (as shown). The wedge also can be used to raise the heel and toe. (Wedge courtesy Norman G. Ducharme, Ithaca, New York.)

To perform the stifle valgus stress test, the clinician’s shoulder (or hand) is used as a fulcrum against the distal femur, and the distal limb is pulled laterally several times before the horse is trotted (see Figure 6-25). False-positive results can be obtained because the entire distal extremity is manipulated during this test. Valgus or varus stress tests can be used in many joints in the distal limb, particularly the interphalangeal joints. Patellar manipulation followed by trotting (see Figure 6-26) may be helpful but can be difficult to perform when horses resist forced proximal movement of the patella (frequently, the veterinarian’s wrist is forced into hyper­ extension). Although cranial and caudal draw tests can be used to exacerbate stifle lameness, I have not found them particularly helpful, and they are dangerous to perform.

FLEXION TESTS AND DIAGNOSTIC ANALGESIA I do not generally recommend combining the results of flexion tests and diagnostic analgesia (called “blocking the flexion test”). I often hear that baseline lameness abated after a block, but the horse still had positive flexion test results. My usual comment is, “Why bother to flex the horse if baseline lameness has been abolished?” Flexion tests induce lameness that may be unrelated to the baseline lameness, a concept that is confusing to the inexperienced and to lay people. Thus it is not unusual that a horse might have residual lameness after flexion, even if the baseline lameness has been eliminated.4 I usually do not recommend further investigation once baseline lameness has been eliminated.

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If baseline lameness is not obvious but a low-grade gait deficit is present, or if a horse has bilaterally symmetrical lameness, flexion tests or other forms of manipulation or provocation may be the only way of “seeing” lameness. In this instance, induced lameness from manipulation can be

assumed to be the baseline lameness, and diagnostic analgesia can proceed. All involved parties should be well informed about the potential for misdiagnosis, but in certain circumstances this pathway may lead to a successful diagnosis.

Chapter

9 

Applied Anatomy of the Musculoskeletal System Matthew Durham and Sue J. Dyson

References on page 1257

It is beyond the scope of this book to describe all aspects of musculoskeletal anatomy in depth, yet a detailed knowledge of anatomy is fundamental to a lameness diagnostician, as highlighted in the chapters on observation and palpation (see Chapters 5 and 6). Some aspects of anatomy are considered in depth in individual chapters dealing with conditions of specific areas. This chapter considers some philosophical aspects of the importance of anatomical knowledge and describes some basic principles. It also provides illustrations that we hope will help the reader to understand better the three-dimensional aspects of anatomy. Accurate interpretation of what we see and feel during an examination requires knowledge of what structures we are looking at and palpating. For example, a swelling is noted over the dorsal aspect of the carpus. Is the swelling diffuse and possibly related to a hygroma, periarticular edema, or cellulitis, or is there a discrete swelling, horizontally oriented, reflecting distention of the middle carpal joint? Or is it a longitudinal swelling reflecting distention of the common digital extensor tendon sheath or the tendon sheath of the extensor carpi radialis? If the swelling is longitudinal, are any compressions in the swelling caused by normal retinaculum or adhesions within the sheath (Figure 9-1)? If we examine the sheath by ultrasonography, is the echogenic band extending from the sheath wall to the enclosed tendon normal mesotendon, or is it an adhesion? If diffuse swelling is present around the dorsal aspect of the carpus associated with lameness, how can we tell if the middle carpal joint capsule is distended? We need to know that there is a palmar outpouching of the middle carpal joint on the palmarolateral aspect of the carpus, just distal to the accessory carpal bone. Thus during visual inspection and palpation the clinician should be constantly asking, “What structure am I seeing or palpating, what are its functions, and what would be the consequences of loss of function?” If it has abnormal contour or size, is this the result of swelling of that structure or of an adjacent or underlying structure? Having established what structure is abnormal, the clinician then must consider the best imaging modality. If it is a tendonous or ligamentous

structure, ultrasonography probably will provide the most information, but we must remember that it has bony attachments, and damage at those attachments might best be assessed by either radiology or nuclear scintigraphy. So we need to know not only what each structure is, but also the structures to which it is attached. During visual inspection and palpation, we also need to think logically. We know that the superficial and deep digital flexor tendons (SDFT, DDFT), the accessory ligament of the DDFT (ALDDFT), and the suspensory ligament (SL) lie on the palmar aspect of the third metacarpal bone (McIII) (Figure 9-2). Swelling confined to just the medial aspect of the metacarpal region is far more likely to reflect direct trauma to the medial aspect of the limb than sprain or strain of any of the ligamentous or tendonous structures. We need to know that the proximal aspect of the SL lies between the bases (heads) of the second and fourth metacarpal bones and therefore is inaccessible to direct palpation, and that desmitis often may be present without discernible soft tissue swelling (Figure 9-3).

ECRT ICB

C3

Fig. 9-1  •  Sagittal anatomical section through the carpus, transecting the extensor carpi radialis tendon (ECRT). C3, Third carpal bone; ICB, intermediate carpal bone.

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SDFT DDFT ICL

SL

A

B

A

Fig. 9-2  •  Sagittal views of the palmar metacarpal region. Proximal is to the right. A, FreeStyle Extended Imaging (Sequoia model, Acuson, Mountain View, California, United States) ultrasonographic image of the palmar metacarpal region. B, Corresponding anatomical section. DDFT, Deep digital flexor tendon; ICL, accessory ligament of the DDFT (inferior check ligament); SDFT, superficial digital flexor tendon; SL, suspensory ligament.

We must be aware of anatomy to realize the possible consequences of trauma to an area. The paucity of soft tissues over the cranial aspect of the stifle makes the patella and the tibial tuberosity vulnerable to direct trauma, hence the risk of fracture after hitting a fixed fence. The lack of soft tissues also means that if the horse hits a thorn hedge, the possibility of a thorn penetrating the femoropatellar joint capsule, resulting in contamination and infection, is quite high. We also need to think about how structures move relative to one another while the horse is in motion. If a steeplechase horse sustains an interference injury on the palmar aspect of the metacarpal region while galloping, the position of the skin laceration probably will not coincide with the level of the laceration in the SDFT (Figure 9-4). We also need to know the relative positions of the laceration and the digital flexor tendon sheath to be aware of the likelihood that the sheath may have been traumatized, and thus the risk of infectious tenosynovitis. Faced with a contaminated wound on the dorsal aspect of a hind fetlock and severe lameness, and the possibility of infection of the metatarsophalangeal joint, we need to know where to expect to see distention of the plantar pouch of the joint capsule and to know that this site is safely accessible for arthrocentesis. A fundamental principle of lameness investigation is the identification of the source or sources of pain. Although this may be possible through detailed clinical examination, in many instances it is essential to perform diagnostic analgesia (see Chapter 10). A detailed knowledge of the anatomy of nerves, joint capsules and the various outpouchings, tendon sheaths, and bursae is fundamental to

SL

ICL DDFT SDFT

B Fig. 9-3  •  Transverse sections through the proximal metacarpal region. Dorsal is to the top and lateral is to the left. A, Anatomical specimen. B, Computed tomographic scan using soft tissue windowing. DDFT, Deep digital flexor tendon; ICL, accessory ligament of the deep digital flexor tendon (inferior check ligament); SDFT, superficial digital flexor tendon; SL, suspensory ligament.

safe, accurate performance of perineural and intrasynovial injections. Given the knowledge of the close relationship among the distal interphalangeal joint capsule, the distal sesamoidean impar ligament, the collateral sesamoidean ligaments and the distal phalanx, and the close proximity of branches of the palmar digital nerve, it is not surprising that intraarticular analgesia is not specific and that other structures

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SL

MC3

SDFT

P1 NF

P2 Fig. 9-4  •  Lateral scintigraphic image of the metacarpal region acquired before the end of the flow (vascular) phase and at the beginning of the pool phase. This jumper had a history of low-grade chronic desmitis of the proximal aspect of the suspensory ligament (SL), and mild diffuse superficial digital flexor (SDFT) tendonitis. An acute interference injury to the midmetacarpal region was evident on the skin. Note the proximal location of the acute injury to the SDFT. The linear area of uptake between the SL and SDFT is vascular artifact related to the time of acquisition.

can be affected, especially if interpretation of the response is delayed or an excessively large volume of local anesthetic solution is used. Knowledge that the medial and lateral femorotibial joints do not normally communicate and that the cruciate ligaments usually are extraarticular structures is crucial for an understanding of why these joint compartments must be injected separately, and why the response to intraarticular analgesia may be both incomplete and delayed if a cruciate ligament is damaged. Knowledge of functional neuroanatomy also is important for interpretation of specific gait abnormalities. Inability to bear weight on a hindlimb after general anesthesia may be the result of myopathy, but in the absence of marked pain and distress, it is more likely that the horse has lost extensor function and is unable to extend any of the hindlimb joints because of femoral nerve paresis. Loss of ability to extend the elbow may result from loss of triceps function associated with a fracture of the olecranon but may also be caused by radial nerve paresis. Vascular anatomy is important because many nerves lie close to vessels. With superficial nerves and vessels, identification of the vessel may facilitate palpation of the nerve and thus aid accurate perineural injection. Avoiding penetration of the vessel and causing hematoma formation also is desirable. With regard to deeper nerves the veterinarian may benefit by knowing that the needle must be in close proximity to the nerve if blood appears in the needle hub. This information can be helpful when performing perineural analgesia of the deep branch of the fibular nerve. Assessment of digital pulse amplitudes is an integral part of palpation. Increased pulse amplitude usually signifies a site of inflammation at, or distal to, the region of

Fig. 9-5  •  Sagittal anatomical section through the pastern demonstrating a common location for the nutrient foramen (NF) entering the proximal phalanx (P1). MC3, Third metacarpal bone; P2, middle phalanx.

palpation, especially in association with inflammatory conditions of the foot, such as subsolar abscessation or laminitis. Palpation of the pulse in the dorsal metatarsal artery and assessment of saphenous vein filling can be helpful in the evaluation of a horse with suspected aortoiliac thrombosis. Knowledge of the sites of major vessels is important when considering the consequences of major laceration to an area and possible avascular areas, and in planning a surgical approach to an area. All bones have one or more nutrient foramina through which major vessels enter. These usually are in standard locations (Figure 9-5). Knowledge of these sites is critical for accurate radiological interpretation because a nutrient foramen appears as a radiolucent area, which should not be confused with a pathological lesion. The position of these intraosseous vessels also has important consequences in considering repair of major long bone fractures. Thermography relies on the detection of surface heat and is obviously greatly influenced by the position of superficial vessels. Interpretation may be misleading without knowledge of location. Thus it should be absolutely clear that anatomy is a dynamic subject and is not merely a function of knowing the origins and insertions of numerous structures. We also need to know some fundamentals of biomechanics. What is the biomechanical function of the SL? What are the implications of loss of function? For example, how may function be altered by a change in foot angle after application of a heel wedge? How is load in the distal limb

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91

SB

B PSB

SDSL

DDFT

SDFT branch

ODSL B

ODSL P2

A

C

C

Fig. 9-6  •  The oblique distal sesamoidean ligaments. A, Frontal magnetic resonance image (MRI) of the pastern showing the origins and insertions of the oblique distal sesamoidean ligaments (ODSL). B, Frontal (left) and transverse (right) ultrasonographic images of the ODSLs obtained at point B in A. Proximal and dorsal are to the left. C, Transverse MRI scan obtained at point C in A. DDFT, Deep digital flexor tendon; P2, middle phalanx; PSB, proximal sesamoid bone; SB, suspensory branch; SDFT, superficial digital flexor tendon; SDSL, straight distal sesamoidean ligament. (A Courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania, United States.)

joints affected by mediolateral foot imbalance? If the accessory ligament of the SDFT is cut (superior check desmotomy), how does this alter the function of not only the SDFT but also other tendonous and ligamentous structures? Does consequent overload of the SL predispose to an increased risk of suspensory desmitis? When orthopedic surgery is being considered, which is the tension side of the bone, to which a bone plate should be applied to take advantage of the tension band principle? In more general terms, how will lameness in the left hindlimb alter forces in the other limbs, and does this vary with the gait? Given the reciprocal apparatus of the hindlimb and the inability to flex and extend the limb joints independently, it is not surprising that the gait characteristics of hindlimb lameness are so similar, irrespective of the source of pain causing lameness. Understanding the reciprocal apparatus in addition to the results of loss of its function (e.g., after damage to the fibularis tertius) is hugely important for an understanding of hindlimb lameness. After the source of pain causing lameness has been isolated, then it is necessary to establish what is causing pain; this requires one of a number of imaging modalities: radiography, ultrasonography, nuclear scintigraphy, magnetic resonance imaging (MRI), computed tomography (CT), and exploratory arthroscopy, bursoscopy, or tenoscopy. Accurate interpretation of the findings from any of these techniques requires specialist anatomical knowledge.

With radiographic images, various structures are super­ imposed, resulting in potentially confusing radiolucent lines that can mimic a fracture (e.g., in the relatively complex carpus and tarsus). A frog shadow superimposed over the navicular bone may mimic a fracture. We must be cognizant of anatomical variations, for example, the shape and size of the crena of the distal phalanx. We have to know how best to image a specific anatomical location, such as the sustentaculum tali of the calcaneus (fibular tarsal bone) using a skyline projection. For interpretation of the clinical significance of periosteal or entheseous new bone, detailed knowledge of the soft tissue structures that do (or do not) attach in that area is vital. Particularly in the fetlock and pastern areas, numerous ligamentous structures have discrete areas of attachment (Figure 9-6). Radiography requires the awareness that we are looking at a three-dimensional structure in two dimensions, and thus images of the area must be obtained from several different angles. With ultrasonography, and more particularly with MRI and CT, structures can be imaged in three dimensions; this requires detailed knowledge of the shape, size, and relationships among structures. In the proximal metatarsal region the DDFT lies more medial than the SDFT and SL, and thus these structures cannot be imaged adequately by ultrasonography at the same time from the plantar aspect of the limb (Figure 9-7). The transducer must be moved to a plantaromedial site to evaluate the DDFT in its

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PART I  Diagnosis of Lameness hindlimb, and presents correlative illustrations of anatomical specimens and images of those areas to assist in the understanding of three-dimensional anatomy.

THE LANGUAGE OF ANATOMY

MT3

The system described in the Nomina Anatomica Veterinaria (NAV) according to the guidelines of the International Committee on Veterinary Anatomical Nomenclature has been used so that anatomical terminology is universal. English translations of NAV terms have been used whenever possible according to these guidelines. MT2

MT4

SL DDFT SDFT

Fig. 9-7  •  Transverse anatomical section of the proximal metatarsal region demonstrating the lateral position of the superficial digital flexor tendon (SDFT) relative to the deep digital flexor tendon (DDFT). Lateral is to the left and dorsal to the top of the image. This arrangement is the opposite of that seen in the forelimb (compare with Figure 9-3). MT2, MT3, and MT4, Second, third, and fourth metatarsal bones, respectively; SL, suspensory ligament.

entirety. A large vessel on the plantarolateral aspect of the SL can cause shadowing artifacts in the SL. The internal architecture of the joint becomes important during exploratory arthroscopy. What are the normal variations in cartilage thickness? Where do you expect to see a synovial fossa? Which parts of the synovial membrane are usually more vascular? Is it normal that the cranial cruciate ligament can be seen without synovial covering from the medial femoral tibial joint? A textbook of this type cannot possibly provide detailed descriptions of all aspects of anatomy, functional anatomy, and biomechanics, nor answer all of the questions posed earlier in this chapter. It is hoped that this overview will stimulate readers to have a thirst for more knowledge of these subjects, in the understanding of their huge importance. Lameness clinicians are encouraged to acquire a set of boiled-out bones for reference and perform detailed dissections of cadaver limbs to improve knowledge of anatomy. Practicing nerve block techniques on cadaver limbs is very important for inexperienced clinicians or those performing a new block for the first time. If a lame horse must be humanely destroyed, clinicians should take the opportunity, whenever possible, to perform a postmortem examination to correlate clinical findings with the actual lesions and revise anatomy at the same time. Each time a dissection is performed, new anatomical detail becomes apparent that previously may have been missed. The remainder of this chapter provides some basic definitions of anatomical terms used elsewhere in the book, describes the reciprocal apparatus of the forelimb and

FORCES The interaction of anatomical structures allows for the conversion of chemical energy into purposeful movement. It is often useful to think of complex anatomical structures in terms of interactions between simplified structural units. The interaction of forces within these anatomical units dictates the abilities and the potential weaknesses of the equine athlete. In simple terms, the stresses acting on the body are compression, tension, shear, torsion, and bending. Compression is the force applied between two points to move them together. Examples of compression are seen in joints, such as within the middle carpal joint at the interface between the radial and third carpal bones, or the compression sustained by the digital cushion between the sole, frog, and the distal phalanx. Compression also is sustained within most bones, such as the third carpal bone or the dorsal cortex of the McIII. Tension is the force that tends to stretch or elongate a structure. Examples of tension are most obvious in tendons and ligaments, but bones such as the olecranon or within the palmar cortex of the McIII also sustain tensile strain. Shear is a stress at the interface between two structures moving in opposite directions. Examples of shear are seen in the femoropatellar and tarsocrural joints, within bone, and within the hoof capsule. Torsion is the stress produced when a twisting motion is applied to an object. Examples of torsional stress are seen within joints, such as the distal hock joints, or within individual bones, such as the McIII. Bending is a combination of compression on one side of a structure and tension on the other side. Structures subjected to bending are long bones such as the McIII, where the dorsal cortex is subjected to compression, whereas the palmar cortex is subjected to tension.

SPECIALIZED STRUCTURES Synovial Structures

Synovial bursae, tendon sheaths, and joints have a similar function and generally similar structure. All are sacs containing synovial fluid produced by the lining of the sac. In simple terms, synovial structures facilitate the movement between independent structures by providing a hydraulic cushion of viscous fluid that limits the effects of friction to help dissipate compressive and shear forces. (For a more complete discussion on synovial structures, see Chapters 61 to 67 and 74 to 79.)

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93

Tibia

Calcaneus

DDF

Gastrocnemius

A Calcanean bursa SDFT Fig. 9-8  •  Transverse anatomical section through distal aspect of the tibia and proximal aspect of the calcaneus demonstrating the distinct calcanean bursa bounded by the collateral ligaments of the superficial digital flexor tendon (SDFT). DDF, Deep digital flexor muscle. PSB

A diarthrosis is a mobile joint containing a synovial membrane. This membrane is flexible enough to allow for movement of the joint. The synovial fluid lubricates, hydraulically equalizes pressure between cartilage plates, and nourishes the articular cartilage. A synovial sheath is a sac that completely surrounds a tendon, forming a synovial lining on the surface of the tendon and the lining of the sheath. The synovial reflection between these visceral and parietal layers is termed the mesotendon. This structure is similar to the mesentery in the abdominal cavity. Nerve and blood supply to the tendon is found within the mesotendon. In areas of great mobility within the synovial sheaths, the nerve and blood supply to the tendons is through a vinculum, which is a modified mesotendon in the form of a narrow band connecting visceral and parietal layers. A synovial bursa is a simple sac lying between a tendon or muscle and an adjacent bony prominence. A bursa does not surround the tendon but acts as a cushion at the interface where pressure is concentrated (Figure 9-8).

Intercalated Bones

Intercalated bones are bones that arise within tendons or ligaments allowing for the interface between the tendonous structure and the underlying bone at an area of focal pressure, typically at the level of a joint. The interface between these bones is within a synovial sac. The navicular bone, proximal sesamoid bones (PSBs), and patella are intercalated bones. These bones allow for smooth movement and dissipation of focal pressure between the tendon or ligament and the underlying joint (Figure 9-9).

ODSL

B Fig. 9-9  •  A, Oblique radiographic image of a normal proximal sesamoid bone (PSB). B, Parasagittal anatomical section through suspensory branch, PSB, and oblique distal sesamoidean ligament (ODSL).

Fibrocartilaginous Structures In general terms, there are four functional arrangements of fibrocartilage: interarticular, connecting, circumferential, and stratiform.

Interarticular Fibrocartilage

Menisci are fibrocartilaginous structures located between the articular cartilages of a diarthrosis. Menisci are not directly attached to the joint surfaces but are held in place by ligaments immediately adjacent to the articular surfaces. They provide congruency between the condyles, allow for a greater range of movement of the joint, and absorb concussion. Menisci are found in the stifle and temporomandibular joints of the horse.

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PART I  Diagnosis of Lameness

Connecting Fibrocartilage

A symphysis is a fibrocartilaginous joint that allows minimal movement. The pelvic symphysis and intersternebral and intervertebral joints are examples of fibrocartilaginous joints.

Serratus ventralis thoracis muscle

Circumferential Fibrocartilage

In the coxofemoral joint the acetabular lip (labrum acetabulare) is a fibrocartilaginous ring extending the articular surface in a firm, semiflexible manner. The transverse acetabular ligament is the portion of the labrum crossing the acetabular notch. The glenoid labrum seen in other species is a poorly developed fibrous band in the shoulder of the horse.

Stratiform Fibrocartilage

Stratiform fibrocartilages arise within ligamentous structures at an interface with high focal pressure between soft tissue and bone, either within a ligament or as an extension of a bony surface. These structures are similar to intercalated bones in that they typically provide rigidity to help dissipate compressive forces, but the moderate elasticity allows for some flexibility of the structures. The parapatellar fibrocartilage on the medial aspect of the patella, portions of the biceps brachii tendon of origin within the intertubercular (bicipital) bursa, the manica flexoria, and portions of the DDFT adjacent to the proximal aspect of the middle phalanx are examples of stratiform cartilage formation within tendonous structures. The proximal, middle, and distal scuta are stratiform fibrocartilaginous structures associated with the intersesamoidean ligament, the palmar aspect of the middle phalanx, and the collateral sesamoidean ligaments, respectively. These structures serve as semirigid pulleys primarily for the DDFT.

PASSIVE STAY APPARATUS Distal Limb

The horse is uniquely equipped to be able to stand at rest while expending minimal muscular effort. In the forelimb and hindlimb the fetlock is prevented from overextension by a combination of structures providing passive resistance. The suspensory apparatus is the main contributor, forming a sling that maintains the fetlock in extension. In addition, the SDFT, DDFT, and the associated accessory (check) ligaments (in the forelimb) act as tension bands providing passive support. The suspensory apparatus consists primarily of the SL and branches, PSBs, and distal sesamoidean ligaments. The intercalated PSBs provide a broad face at the point where focal pressure is high at the palmar or plantar aspect of the fetlock joint, enabling the ligamentous tension band to support the fetlock. Dorsal branches of the SL join with the common or long digital extensor tendon, helping to stabilize the dorsal aspect of the digit. The axial and abaxial palmar and plantar ligaments of the proximal interphalangeal joint, the SDFT branches, and the straight sesamoidean ligament support the palmar or plantar aspect of the proximal interphalangeal joint. The navicular bone and its suspensory apparatus, in combination with the distal sesamoidean impar ligament, stabilize the palmar or plantar aspect of the distal interphalangeal joint.

Biceps brachii muscle

Triceps brachii muscles

Lacertus fibrosus Extensor carpi radialis muscle

Common digital extensor tendon

Fig. 9-10  •  The passive stay apparatus of the forelimb.

Forelimb

In the forelimb the fibrous portion of the serratus ventralis thoracis acts as a sling suspending the thorax from the forelimb by its attachment to the scapula. The downward force applied by the serratus ventralis on the caudal aspect of the scapula causes slight flexion of the scapulohumeral joint, applying tension to the biceps brachii. A fibrous band of the biceps brachii extends from the supraglenoid tubercle of the scapula and continues as the lacertus fibrosus, which joins with the extensor carpi radialis to passively extend the carpus. Minimal muscular effort by the triceps on the olecranon maintains the elbow in extension (Figure 9-10).

Hindlimb

The stifle is maintained in extension by the patellar locking mechanism with minimal muscular effort. Slight muscular effort by the quadriceps and tensor fasciae latae rotates the patella medially, where the cartilaginous process of the

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95

Tensor fascia lata

Patella

Lateral patellar ligament Middle patellar ligament Medial patellar ligament

Middle and medial patellar ligaments

Lateral fibrous band of gastrocnemius Peroneus (fibularis) tertius and long digital extensor

Medial collateral ligament Peroneus (fibularis) tertius Tibial crest

Long digital extensor muscle

SDFT DDFT

Fig. 9-11  •  The patellar locking mechanism.

patella is caught caudal to the large prominence of the medial trochlear ridge of the femur. Slight relaxation of the quadriceps as a whole allows slight flexion of the stifle, which “locks” the patella in place by applying tension primarily to the medial and middle patellar ligaments (Figure 9-11). When the stifle is extended, the hock is passively extended by the superficial digital flexor and the fibrous component of the lateral head of the gastrocnemius muscles, which extend from the femur to the tuber calcis. The reciprocal apparatus forces the hock to flex and extend in unison with the stifle. The reciprocal apparatus transfers mechanical energy to the distal aspect of the limb from the massive muscular structures of the upper limb without adding mass to the lower limb. The superficial digital flexor and the fibrous portion of the gastrocnemius muscles serve as the caudal component of the reciprocal apparatus, along with the long plantar ligament, which acts as a tension band to make the calcaneus, distal aspect of the tarsus, and metatarsal region a single functional lever arm. The fibularis (peroneus) tertius serves as the cranial component of the reciprocal apparatus, extending from the femur to the dorsal and lateral aspects of the tarsus (Figure 9-12). Although the fibularis tertius is important as part of the reciprocal apparatus, it is not essential for function of the passive stay apparatus, because its function is flexion of the tarsus.

Fig. 9-12  •  The reciprocal apparatus. DDFT, Deep digital flexor tendon; SDFT, superficial digital flexor tendon.

A second reciprocal mechanism has been described for the lower hindlimb, where the fetlock and digit are flexed at the same time as the stifle and hock. The long digital extensor tendon and DDFT were the dorsal and plantar components suggested, but the SDFT probably also contributes.

THREE-DIMENSIONAL ANATOMY Major advances in lameness diagnosis are being made with the assistance of advanced imaging techniques. Radiography, nuclear scintigraphy, and ultrasonography are well established, whereas CT and MRI are growing in importance. CT and MRI in particular require a detailed knowledge of three-dimensional anatomy. It is beyond the scope of this text to provide detailed correlative images of the entire musculoskeletal system. Figures 9-13 through 9-18 give a flavor of what is possible. Figures 9-13 through 9-16 highlight the complex anatomy of the navicular Text continued on p. 100

DFTS

DSCL

DIP P2

P3 Nav

A

DSIL

NB

B

DDFT

D,E

DDFT DSCL DFTS

P2 DIP Nav

F

C

D

DDFT

NAV BONE

E

F

DDFT

NAV BONE

Fig. 9-13  •  Comparisons of the lateral view of the navicular bone and its relationship to neighboring structures. A, Sagittal anatomical section showing the digital flexor tendon sheath (DFTS), navicular bursa (NB), and distal interphalangeal (DIP) joint surrounding the navicular bone. B, Lateromedial radiographic image centered on the navicular bone. C, Sagittal magnetic resonance imaging scan of the foot. D and E, Sagittal anatomical section and corresponding ultrasonographic image of the palmar aspect of the distal aspect of the pastern obtained at points D and E in panel C. Proximal is to the right. The arrows outline the distal sesamoidean collateral ligament. F, Frontal (left) and sagittal (right) ultrasonographic images obtained through the frog at point F in panel C. The hypoechoic appearance of the portion of the deep digital flexor tendon (DDFT) is caused by the off-incidence artifact because the fibers are not perpendicular to the line of the ultrasound beam. Lateral and proximal are to the right. DSIL, Distal sesamoidean impar ligament; DSCL, distal sesamoidean collateral ligament (axial union forming fibrous portion of T ligament); Nav, navicular bone; P2, middle phalanx; P3, distal phalanx. (B Courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania, United States.)

Chapter 9  Applied Anatomy of the Musculoskeletal System



A DDFT

B

Nav bone

C Fig. 9-14  •  Transverse sections through the navicular bone. A, Anatomical specimen, palmar view. B, Palmaroproximal-palmarodistal oblique radiographic image of a normal navicular bone. C, Transverse magnetic resonance image. The deep digital flexor tendon (DDFT) is nearly as broad at this point as the navicular bone. (Courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania, United States.)

P2

DSCL

A

p DDFT

t

B Fig. 9-15  •  Transverse sections through the foot at the level of the distal sesamoidean collateral ligaments (DSCL). A, Anatomical section showing the attachments of the DSCL to the deep digital flexor tendon (DDFT) marked at point t, and to the middle phalanx (P2) at point p. These attachments form the so-called “T ligament,” which forms the boundaries between the navicular bursa, distal interphalangeal joint, and digital flexor tendon sheath.  B, Corresponding magnetic resonance image. (Courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania, United States.)

97

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PART I  Diagnosis of Lameness

DSIL insertion

ft fs (DDFT insertion)

A

B

ft

C

D

Fig. 9-16  •  The insertions of the deep digital flexor tendon (DDFT) and distal sesamoidean impar ligament (DSIL). A, Isolated distal phalanx solar view, showing the point of insertion of the DDFT on the flexor surface (fs). The flexor tubercle (see ft in panel C) is relatively smaller than in other species but should be recognized as a normal structure as seen on computed tomographic (CT) imaging. B, Transverse anatomical section through the insertion of the DDFT. This slice is slightly distal to the site of insertion of the distal sesamoidean impar ligament. C, Transverse CT image showing a normal flexor tubercle (ft). Avulsions here are difficult to demonstrate radiologically. Nuclear scintigraphy and ultrasonography can be helpful, but this area is best imaged using CT or magnetic resonance imaging (MRI).  D, Transverse MRI scan. (D courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania, United States.)

Chapter 9  Applied Anatomy of the Musculoskeletal System



Joint capsule

ECRT

CDET ICB

UCB RCB Medial palmar nerve

Accessory carpal bone

C

DDFT

Median artery

Carpal canal

A

ACB

DDFT

SDFT

SDFT

B

D Fig. 9-17  •  Transverse slices through the proximal row of carpal bones. All images are oriented with dorsal to the top and lateral to the left. A, Diagram of carpal bones. B, Anatomical section. C, Magnetic resonance imaging image. D, Computed tomographic image. ACB, Accessory carpal bone; CDET, common digital extensor tendon; DDFT, deep digital flexor tendon; ECRT, extensor carpi radialis tendon; ICB intermediate carpal bone; RCB, radial carpal bone; SDFT, superficial digital flexor tendon; UCB, ulnar carpal bone. (C Courtesy Alexia L McKnight, University of Pennsylvania, Philadelphia, Pennsylvania, United States.)

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PART I  Diagnosis of Lameness

ECRT

ICB

C3

A

B Fig. 9-18  •  Lateral views of the carpus. Compare with Figure 9-1. A, Flexed lateromedial radiographic image. B, Flexed sagittal magnetic resonance imaging image through the extensor carpi radialis tendon (ECRT). C3, Third carpal bone; ICB, intermediate carpal bone. (Courtesy Alexia L McKnight, University of Pennsylvania, Philadelphia, Pennsylvania, United States.)

bone region, showing the close relationship between the collateral sesamoidean ligaments, the distal sesamoidean impar ligament, the DDFT, and the navicular bursa and

distal interphalangeal joint capsule. Figures 9-17 and 9-18 demonstrate the relationship among some aspects of the complex anatomy of the carpal region.

Chapter

10 

Diagnostic Analgesia Lance H. Bassage II and Mike W. Ross

Despite the many technological advances in equine sports medicine over the past three decades, diagnostic analgesia arguably remains the most valuable tool in the equine clinician’s arsenal to localize pain causing lameness. Although the technique requires a thorough understanding of anatomy, basic technical skill, and clinical experience, the equipment and expense are minimal. In addition, diagnostic analgesia can be performed on site, with the outcome immediately obvious. Any lingering concern that a suspected “shoulder problem” exists is convincingly erased when the response to perineural analgesia of the digit is observed. This chapter reviews the various perineural, intrasynovial, and local (regional) infiltration techniques for application of local analgesia in the diagnosis of lameness in horses.

LOCAL ANESTHETICS: PHARMACOLOGY AND TISSUE INTERACTIONS Pain is transmitted specifically in the small, lightly myelinated, A delta and nonmyelinated C nerve fibers.1 All commonly used local anesthetic solutions, regardless of the specific molecular structure, share the same basic mechanism of action—specifically, the ability to block or inhibit nociceptive nerve conduction by preventing the increase in membrane permeability to sodium ions.2 These agents consist of a lipophilic and a hydrophilic group, connected by an intermediate chain containing a carbonyl group of an amide or ester linkage, and have traditionally been categorized as either amide- or ester-type local anesthetics.3 Common local anesthetic solutions used in horses—2% solutions of lidocaine, mepivacaine, and bupivacaine—are of the amide type. Compared with most local anesthetics, lidocaine and mepivacaine are considered relatively fast-acting and have a reported duration of action of 11 2 to 3 hours and 2 to 3 hours, respectively. In contrast, bupivacaine is intermediate in onset but has a much longer duration of action (3 to 6 hours).4 Bupivacaine is most suited for providing therapeutic rather than diagnostic analgesia. The results in

References on page 1257

clinical practice vary, because in severely lame horses the degree and duration of local analgesia are decreased, regardless of the agent used. When local anesthetic solutions are injected, tissue damage can occur but is extremely rare.3,4 Soft tissue swelling occurs occasionally and is likely caused by needle trauma or hematoma formation and not from a direct drug-tissue interaction. We suggest that alcohol and a clean wrap be applied to the injection sites when the diagnostic evaluation is complete to prevent or minimize swelling at injection sites. Cellulitis or other forms of infection are rare potential complications. Acute synovitis, or flare, is a rare complication that can occur after intrasynovial (most commonly intraarticular) injection of local anesthetic solutions. Synovitis from intrasynovial injection of local anesthetic solution is much less common than from injection of other medications. Mepivacaine is thought to be less irritating than lidocaine when administered intraarticularly, but we have not recognized this difference.3 However, Dyson reported that lidocaine may be considerably more irritating than mepivacaine, and clinical data documenting differences were used successfully in the licensing of mepivacaine in the United Kingdom.5 Like cellulitis after perineural injections of local anesthetic solutions, infectious synovitis is a rare but possible sequela. To mitigate the possibility of contaminated solution, we use a new vial of local anesthetic solution when performing intrasynovial analgesic procedures. Systemic side effects from diagnostic analgesic techniques are exceedingly rare. Cardiovascular or central nervous system signs, including muscle fasciculation, ataxia, and collapse, were reported.3 Systemic intoxication would require a dose much higher than is commonly used, even for an extensive diagnostic evaluation. For example, the maximum single infiltration dose of lidocaine that can be safely administered to a 500-kg horse is about 6.0 g, or 300 mL of a 2% solution.6

Strategy, Methodology, and Other Considerations

A few basic principles must be followed to ensure success. A thorough working knowledge of regional anatomy is required. Even for seasoned veterans a review of anatomy may be required before less common techniques are performed. A most important principle when performing perineural analgesia is to start distally in the limb and work proximally (Figures 10-1 to 10-4). If possible, sequential blocks from distal to proximal should always be used, but in certain circumstances a different strategy can be successful. Sequential blocking requires a fair amount of time, and in certain horses, selective intraarticular or local blocks can be performed without following this “golden rule.” However, in most situations, blocking a large portion of the distal limb at a proximally located site may preclude accurate determination of the source of pain causing lameness and may require an additional visit to perform additional diagnostic procedures. It is important to test the efficacy of a perineural block before reevaluating the horse’s degree of lameness. If any question exists, the block should be repeated rather than assuming deep pain has been abolished, when skin sensitivity persists. If a horse shows partial improvement only minutes after injection, an additional few minutes should be allowed for complete analgesia to be achieved before

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101

proceeding with the next block. Alternatively, the block can be repeated. In so doing, the clinician minimizes the potential for misinterpretation and the tendency to ascribe the residual lameness to a “second problem” that does not exist. During this portion of the examination, we are attempting to eliminate baseline rather than induced lameness, and care must be taken when adopting the practice of “blocking out a positive flexion test” (see Chapter 8). Once baseline lameness has been eliminated, we rarely perform additional flexion tests or attempt to eliminate all induced lameness. How is the efficacy of the block assessed? Several methods are available, but the following points should be considered. Individual horses react differently to noxious stimuli applied to the skin. Therefore it is helpful to test the contralateral (unblocked) limb to establish the horse’s baseline response to the test. Similarly, covering a horse’s eye or feigning a few gestures with an instrument (pen tip, hemostatic forceps) without actually contacting the skin can help differentiate between a random or anticipatory response by an apprehensive horse and a true painful response. Positioning oneself on the contralateral side of the horse when testing for sensation also can help in making this determination. The clinician should avoid using sharp instruments that can penetrate the skin and cause hemorrhage, a situation not well understood by a concerned horse owner. Hemostatic forceps, used to pinch the skin, are ideal, because they are blunt and appear to consistently induce an appropriate amount of pain. Forceps are only useful in assessing superficial or skin sensation, however. Perineural blocks must be assessed for the amelioration of deep and not just superficial pain. To assess whether deep pain in the hoof has been ameliorated after palmar digital analgesia or other techniques, hoof testers can usually be applied with enough force to cause a painful response, even in the most stoic of horses. Physical strength of the operator must be considered. Extreme or hard joint flexion (combined with varus or valgus stress) can be used to assess whether deep pain has been abolished in more proximal locations. In some instances, however, it is impossible to avoid contacting the skin proximal to the site of local anesthetic administration, leading the clinician to assume that the block has not worked. The application of firm digital pressure in the blocked area may be a viable alternative to flexion or manipulation to help avoid these potentially confounding factors. It is important to understand that the region of the limb that is actually desensitized may, in fact, differ from the region the clinician intended to desensitize.7 Proximal diffusion of local anesthetic solution appears to be the most likely cause, but other, intangible factors may play a role. Using a small volume of local anesthetic solution (1 to 5 mL for most perineural blocks) can minimize but not abolish this phenomenon. To further minimize the potential for diffusion of local anesthetic solution, the horse should be reevaluated no more than 10 minutes after the injection (exceptions apply in certain situations). A recent study using 2 mL of radiopaque contrast medium injected perineurally around the palmar nerves at the level of the proximal sesamoid bones demonstrated proximal diffusion extending 2 to 3 cm within 10 minutes of injection, irrespective of whether horses stood still or walked.8

PART I  Diagnosis of Lameness

102

Primary Analgesic Procedure

Anatomical Diagnosis

Final Diagnosis

Differential Procedures

Proceed to Proximal Limb (–) (+)

Middle carpal joint block (–) Wheat block

MC/CMC joint problem Suspensory origin problem (unlikely if Wheat negative) Palmar metacarpal problem Carpal sheath problem

(+)

Osteoarthritis/synovitis Articular fracture

Carpal sheath

(+) (–)

Tenosynovitis/tendonitis Proximal suspensory desmitis Proximal palmar McIII lesion Small metacarpal lesion

(+)

High palmar block

Metacarpal problem Carpal problem (MC/CMC joints)

Wheat block (–) Middle carpal joint block (see above for details) (+)

Digital flexor tendon sheath block

(–) (–)

Dorsal metacarpal disease

(–)

Subchondral bone lesion Extraarticular problem

(–) Low palmar block

(+)

Distal metacarpal problem MCP region problem

MCP joint block

Digital flexor tendon sheath block

(–)

(–)

PIP joint block

Mid-pastern ring block or Abaxial sesamoid block

(+)

(+)

(–) (+)

(–) (+)

Dorsal foot problem Pastern problem

DIP joint block

PIP joint block

DIP joint block

(+)

Foot problem Distal pastern problem

Navicular bursa block

Tenosynovitis/tendonitis (distal aspect DFTS) Dorsal laminar disease Distal sesamoidean desmitis Other soft tissue problem? Fetlock region problem? Osteoarthritis Osteochondrosis P3 Extensor process fracture P3 Midsagittal fracture

(+)

Osteoarthritis Osteochondrosis

(–)

(–) Palmar digital (PD) block

Osteoarthritis/synovitis Osteochondrosis Articular fracture

(+)

(–)

(–)

Tenosynovitis/tendonitis (proximal aspect DFTS)

(+)

Navicular disease Osteoarthritis P3 Fracture Pedal osteitis Soft tissue problem Navicular disease

Fig. 10-1  •  Blocking strategy in the forelimb: foot to carpus. CMC, Carpometacarpal; DFTS, digital flexor tendon sheath; MC, middle carpal; McIII, third metacarpal bone; MCP, metacarpophalangeal; P3, distal phalanx; PIP, proximal interphalangeal.

Complete analgesia, and thus 100% improvement in lameness score, is the goal when performing diagnostic analgesia, but in many horses this level of pain relief is never achieved. Improvement in degree of lameness greater than 70% to 80% after most perineural or intraarticular

techniques should be considered a positive response in most horses. The quintessential response is that the horse “switches lameness” to the contralateral limb, indicating that now pain arising from the opposite limb is greater than the pain that caused the baseline lameness. However,

Chapter 10  Diagnostic Analgesia



Primary Analgesic Procedure

Anatomical Diagnosis

103

Final Diagnosis

Differential Procedures

Proceed to advanced imaging? Cervical vertebral OA? Neurological disease? Reassess?

(–) (+)

Bicipital bursa block

Bursitis Tendonitis Humeral osteitis

Bicipital bursa/tendon problem Proximal humeral problem

(–) (+)

Shoulder joint block

Synovitis Osteoarthritis Osteochondrosis

Shoulder joint

(–) Cubital (elbow) joint block

(+)

Synovitis Osteoarthritis

Elbow joint

(–) (–) Median and ulnar blocks

(+)

Distal antebrachium

Carpal joint blocks Carpal sheath block (see below and Fig.10–1)

(–)

(–)

Antebrachiocarpal joint

(+)

Periarticular soft tissue problem Distal radial trauma/fracture Superior check desmitis/enthesitis Synovitis Osteoarthritis Articular fracture

Antebrachiocarpal joint

Fig. 10-2  •  Blocking strategy in the forelimb: antebrachium to shoulder joint. OA, Osteoarthritis.

complete response may not occur, and the clinician must decide when to stop sequential blocks or when the horse has “blocked out.” The clinician hopes for an obvious difference in lameness score when the horse is blocked, but in some horses, serial improvement occurs with each successive block, a situation that makes assessing the primary source of pain difficult. Incomplete response to local analgesia in some horses may be explained by the fact that chronic pain, particularly deep bone pain, may remain resistant to complete analgesia when perineural techniques are used. For example, horses with laminitis tend to remain lame despite blocking many times at the appropriate level, probably because of neuropathic pain.9 Mechanical gait deficits do not improve after diagnostic analgesia because pain is minimal. Horses may continue to show lameness even with pain abolition, a situation that appears to be caused by habit. These horses tend to show mild residual lameness initially, only to warm out of it quickly during examination. Other factors affecting response to diagnostic analgesia include individual variation in neuroanatomy, the intermittent nature of certain lameness conditions, and the inherent difficulty in assessing and abolishing pain in horses with subtle lameness.10 Articular and subchondral bone lesions may not be desensitized by

intraarticular analgesia, and pain may be more effectively abolished using perineural techniques. Sensory innervation of joints is complex and involves three classes of neurons that transmit information from four receptor types, each of which has a specific distribution throughout the joint.11-13 Articular pain can arise from several sources, including the synovium (inflammation, effusion), fibrous joint capsule (increased intraarticular pressure), articular and periarticular ligaments, periosteum, and subchondral bone (injury, osseous vascular engorgement).10,12,14,15 Other than small branches in the perichondrium, articular cartilage is devoid of innervation. In osteoarthritic joints, however, erosion channels, formed in the calcified layer of cartilage, are invaded by subchondral vasculature.12 Putative nociceptive neurotransmitters were identified in these areas, and therefore it is plausible that in horses with advanced osteoarthritis, pain could be emanating from the deep cartilage layers.16,17 On occasion, lameness from an articular lesion abates after perineural analgesia but shows minimal or only partial response after intraarticular analgesia. In some horses, this can be explained by the fact that pain is originating from articular and periarticular tissues.8 Subchondral bone pain—caused by maladaptive bone remodeling, cystic or erosive lesions, incomplete fractures, and

PART I  Diagnosis of Lameness

104

Primary Analgesic Procedure

Anatomical Diagnosis

Final Diagnosis

Differential Procedures

Proceed to proximal limb (–) Tarsocrural joint block

(+)

Tarsocrural joint problem

Synovitis Osteochondrosis Osteoarthritis Articular fracture

CD joint problem

Osteoarthritis Articular fracture

(–) (+)

CD joint block (–) TMT joint block

(+)

TMT joint problem (± Proximal plantar metatarsal problem?)

Suspensory origin infiltration

(–)

Metatarsal problem Tarsal problem? (TMT, ± CD joints) Tarsal sheath problem?

TMT joint block Tarsal sheath block (see Fig. 10-4)

(–)

(–) High plantar block

(+)

(+)

Digital flexor

(–)

Osteoarthritis Articular fracture Suspensory desmitis Proliferative periostitis MtII/IV Fracture MtIII Other metatarsal problem Tenosynovitis/tendonitis (proximal aspect DFTS)

(–) Subchondral bone lesion Extraarticular problem

(–) Low plantar block

(+)

Distal metatarsal problem MTP region problem

(+)

MTP joint block

(+)

Digital flexor tendon Sheath block

(–)

(–) (–) PIP joint block

Osteoarthritis/synovitis Osteochondrosis Articular fracture

Tenosynovitis/tendonitis (distal aspect DFTS) Dorsal laminar disease Distal sesamoidean desmitis Other soft tissue problem? Fetlock region problem?

(+) Osteoarthritis Osteochondrosis

(–) Mid-pastern ring block or Abaxial sesamoid block

(+)

Dorsal foot problem Pastern problem

DIP joint block

PIP joint block

(–)

(+)

P3 Extensor process fracture P3 Mid-sagittal fracture

(+)

Osteoarthritis Osteochondrosis

(–) Plantar digital block

(+)

Foot problem Distal pastern problem

DIP joint block

(+)

Osteoarthritis P3 Fracture Pedal osteitis Soft tissue problem

Fig. 10-3  •  Blocking strategy in the hindlimb: foot to hock joint. CD, Centrodistal; DFTS, digital flexor tendon sheath; DIP, distal interphalangeal; MtII, MtIII, MtIV, second, third, and fourth metatarsal bones, respectively; MTP, metatarsophalangeal; P3, proximal phalanx; PIP, proximal interphalangeal; TMT, tarsometatarsal.

Chapter 10  Diagnostic Analgesia



Primary Analgesic Procedure

Anatomical Diagnosis

105

Final Diagnosis

Differential Procedures

Proceed to advanced imaging? Pelvic/sacroiliac problem? Back/vertebral problem? Neurological disease? Reassess? (–) (+)

Trochanteric bursa block

Trochanteric bursa problem Gluteal tendon problem Greater trochanter problem

Bursitis Tendonitis Trochanteric osteitis

Coxofemoral joint problem

Synovitis Osteoarthritis Articular fracture

(–) (+)

Coxofemoral joint block

(–) Stifle joint blocks

(+)

Stifle joint problem

Block joints sequentially

(+)

Synovitis Osteoarthritis Osteochondrosis Articular fracture Cruciate/meniscal injury

SBC distal tibia Calcanean tendonitis Distal tibial fracture Other distal crural problem? Calcanean bursa block

(–)

Calcanean bursitis Gastrocnemius enthesitis Osteitis – Tuber calcanei

(–)

Tarsal sheath block

(+)

Tenosynovitis DDF tendonitis Osteitis – sustaculum tali

(+)

Various articular problem (see Fig.10–3)

(–) Fibular and tibial blocks

(+)

Distal crural problem Tarsal problem

Tarsal joint blocks (see Fig.10–3)

Fig. 10-4  •  Blocking strategy in the hindlimb: crus to coxofemoral joint. DDF, Deep digital flexor; SBC, subchondral bone cyst.

osteoarthritis—is inconsistently abolished by intraarticular analgesia. In fact, subchondral bone pain is abolished much more consistently by perineural techniques. Subchondral bone receives innervation from endosteal branches of peripheral nerves that enter the medullary cavity through the nutrient foramen.10,11,18,19 Intraarticularly administered local anesthetic solutions may not penetrate subchondral bone sufficiently to completely block these nerves. This shortcoming is presumably even more likely in situations in which the cartilage is intact. Unfortunately, intraarticular analgesia, although easier to perform, inconsistently abolishes pain from many of the common articular problems. This fact, however, is either overlooked or misunderstood by many practitioners.

Whenever possible, perineural analgesia should be performed, particularly in the distal aspect of the limbs, because this type of analgesia more consistently abolishes pain from all aspects of the joint and surrounding soft tissue structures.

Lameness Is Worse after Diagnostic Analgesia

Two uncommon situations arise when performing diagnostic analgesia. The first occurs during a blocking session. After performing palmar digital analgesia in a horse with forelimb lameness, lameness score may worsen by one or two grades. In fact, lameness may occasionally be considerably worse, prompting concern by the lameness diagnostician. Why? This unusual response occurs most commonly

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in horses with proximal, palmar metacarpal pain caused by proximal suspensory desmitis, avulsion fracture of the proximal palmar aspect of the third metacarpal bone (McIII), or proximally located superficial digital flexor tendonitis. Horses normally shorten the cranial phase of the stride to protect a source of pain, a common response by any lame horse. We reason that after palmar digital analgesia a lack of proprioception in the digit prompts the horse to take a somewhat longer stride, increasing the cranial phase. Compared with before the block an exaggerated load causes the horse to display a higher lameness score. Temporary exacerbation of lameness after palmar digital analgesia can be a useful characteristic to help determine the genuine source of pain. The second situation is more ominous. A horse will occasionally be very lame, sometimes non–weight bearing, once a block wears off. This unusual, but important and sometimes difficult situation occurs when incomplete fractures become separated, displaced, or comminuted. Horses with fractures of the distal phalanx that are incomplete or have healed partially by a fibrous union or those with incomplete fractures of the proximal phalanx appear most at risk. Horses at risk are candidates for imaging before blocking, but in some this complication is unforeseen (see following discussion).

Perception of Diagnostic Analgesia by Laypersons

One of the intangible factors that can complicate the lameness examination is the layperson’s perception of diagnostic analgesia or nerve blocking. In many instances the opportunity for an owner or trainer to observe the outcome of diagnostic analgesia provides the concrete evidence that finally convinces him or her of the diagnosis. The classic example is the suspected acute shoulder injury that is actually chronic navicular disease. However, for many reasons, misunderstanding about diagnostic analgesia can lead to frustration for everyone involved. Many laypersons are not fully able to recognize the baseline lameness and therefore may not be capable of seeing that the horse’s lameness improves after the block. Another difficulty is trying to explain why lameness in a horse with an articular problem is better after a perineural block but no better when local anesthetic solution is placed directly into a joint. Similarly, many laypersons do not understand why a horse with an articular lameness may “block sound” but does not respond satisfactorily to therapeutic injection. This finding that a horse blocks sound but does not “inject sound” is quite common in young racehorses with subchondral bone pain. Most experienced practitioners have learned to deal with these issues, but the new graduate may need fortitude and ingenuity when explaining the results of diagnostic analgesia.

Role of Chemical Restraint

Whenever possible, use of physical (nose or shoulder twitch) rather than chemical restraint is best when diagnostic analgesia is performed. This is particularly important in horses with low-grade lameness. The analgesic properties of α2-agonists (e.g., xylazine, detomidine) and synthetic opiates (e.g., butorphanol) are well recognized and may lead to false-positive results. Ataxia after sedation can complicate lameness interpretation. However, in some horses mild sedation or tranquilization may be necessary

for performance of diagnostic analgesia and may improve the clinician’s ability to evaluate the baseline lameness. Acetylpromazine (0.02 to 0.04 mg/kg intravenously) can calm a highly strung horse and facilitate the lameness examination. Extra care must be taken when performing hindlimb procedures, and the safety of everyone involved and the horse must be considered. In horses with moderate or severe lameness, xylazine (0.15 to 0.30 mg/kg intravenously) may not interfere appreciably with lameness interpretation. Similarly, extremely fractious horses can be sedated with an α2-agonist, which then is reversed with the prescribed α2-antagonist (e.g., yohimbine) before reevaluation. Alternatively, sedation can simply be allowed to wear off before the horse is evaluated, but diffusion of local anesthetic solution may occur or the effect may wear off, both of which may potentially cause misinterpretation of results.

Horse Preparation

Before perineural analgesia is performed, the skin and hair should be cleaned of any gross debris such as mud, bedding, feces, or poultice. Clipping usually is not necessary unless the hair coat is long and prohibits accurate palpation of anatomical landmarks or adequate cleaning of the site. The site should then be scrubbed with an antiseptic, such as povidone-iodine or chlorhexidine, using clean gauze sponges or cotton. If the clinician has any concern about inadvertent penetration of a synovial cavity, a 5-minute aseptic preparation should be performed. This is followed by isopropyl alcohol administration over the site using cotton or gauze sponges. Aseptic preparation should always be performed before any intrasynovial injection. Considerable debate and variation exists among clinicians regarding the need to clip the hair over the site. Some clinicians always clip the hair, whereas others never do. Still others shave the hair in a small area directly over the injection site. The results of a study indicated no significant difference in the number of postscrub colony-forming units (bacterial flora) between clipped and unclipped skin over the distal interphalangeal (DIP) and carpal joints.20 Nonetheless, we still clip the hair over all proposed intrasynovial injection sites before undertaking a 5-minute aseptic preparation. The only time we deviate from this policy is when we are specifically asked not to clip the hair, a situation that arises in some sports horses actively competing, in claiming horses, or in those being sold. Similar variation among clinicians exists regarding wearing of sterile latex gloves when performing an intrasynovial injection. However, we recommend wearing sterile gloves during these procedures. Science aside, clipping hair and wearing sterile gloves project a positive impression to all in attendance. How does, or should, the practitioner attempt perineural or intrasynovial analgesia in a horse with contact or chemical dermatitis (scurf) over the proposed injection site? A superficial wound or abrasion with a localized infection presents a similar quandary. For obvious reasons, these areas are difficult, if not impossible, to clean effectively. If possible, an alternative site, away from the area of dermatitis, should be used. If not, then the procedure should be delayed until the skin condition (or wound) has resolved. In many instances, dermatitis can be treated with topical

medications (medicated sweats such as nitrofurazonedimethylsulfoxide) for a few days to facilitate resolution of the problem.

Injection Techniques

Perineural injections are typically performed using needles ranging in size from 25 gauge, 1.6 cm ( 5 8 inch) to 20 gauge, 2.5 or 4 cm (1 to 11 2 inches). Small needles cause less pain but carry the risk of breaking off within tissues if the horse kicks out or otherwise misbehaves. For this reason, we recommend using 18- or 19-gauge needles for injections or blocks within the proximal metatarsal or plantar tarsal regions. In the distal aspect of the limb the needle is inserted subcutaneously directly over and parallel to the nerve. We generally direct the needle proximally rather than distally, although this portion of the procedure differs among clinicians. One of the Editors (SJD) always inserts the needle distally; if a fractious horse throws the limb to the ground the needle is more likely to stay in situ, and the remainder of the procedure may be completed with the limb on the ground. Directing the needle distally also ensures more distal placement of the local anesthetic solution, which may be important at distal sites. The needle is inserted before the syringe is attached. To avoid excessive manipulation once the needle is inserted, a slip-type syringe hub is preferred. Syringes with screw-on hubs can be difficult to attach, requiring additional manipulation in a sometimes fractious horse, and are not generally used. However, when dense tissue requires that additional force be used for injection, the seal between the hub and the needle can be broken, a complication minimized by using a screw-on hub (see the following discussion of lateral palmar block). Volume of local anesthetic solution varies, but for a majority of blocks in the distal limb, 1 to 5 mL is injected at each site. Larger volumes are used to perform the median and ulnar or fibular (peroneal) and tibial techniques and when infiltrating the proximal palmar (plantar) metacarpal (metatarsal) region. After injection, we briefly massage the sites with gauze sponges or clean cotton soaked in alcohol. Skin sensation and deep pain are assessed 5 to 10 minutes after injection. More time is allowed under certain circumstances (see specific comments throughout the chapter). At the completion of the examination an alcohol wrap should be applied to minimize swelling, a common sequela resulting from local irritation and bleeding from nearby vessels. For “ring” blocks, circumferential subcutaneous infiltration of local anesthetic solution, and other local or regional infiltration techniques, we most commonly use 20- to 22-gauge, 4-cm needles. For performance of a ring block, the needle is inserted perpendicular to the long axis of the limb, and local anesthetic solution is injected as the needle is advanced, leaving a clearly visible wheal or subcutaneous bleb in most locations. The needle then is reinserted at the leading edge of this wheal, a practice that minimizes the number of injections and the horse’s discomfort. However, most horses object to needle insertion even when it is performed well within the bleb. The injection is continued around the limb in this manner. For most ring blocks in the distal limb, 10 to 15 mL of local anesthetic solution is used, but larger volumes may be preferred for surgical procedures. Ring blocks can be done as a

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substitute for or in combination with perineural injections (see the specific blocking techniques discussed in the chapter). However, simply placing local anesthetic solution in a subcutaneous location is not a substitute for the preferred approach, direct perineural injection. To block a local area such as a splint or curb, the needle is typically inserted in one or two locations, and local anesthetic solution is deposited in a fan-shaped pattern. As with the perineural analgesia, the sites are massaged briefly and the horse is reevaluated in 5 to 10 minutes. Intrasynovial injections typically are performed using needles ranging in size from 22 gauge, 2.5 cm to 18 gauge, 4 cm. If marked effusion is present, drainage of synovial fluid is advised, either by allowing the fluid to drip from the hub of the needle or by aspirating with a sterile syringe before proceeding with injection. We prefer the former procedure unless fluid analysis is necessary. The manipulation required to attach the syringe may cause the horse discomfort and potentially dislodge the needle but if successful may hasten withdrawal of synovial fluid. Brief evaluation of the color and viscosity of synovial fluid can shed some light on the disease process within and is expected practice among most racehorse trainers. Volume of local anesthetic solution varies considerably between synovial cavities, but the clinician should keep in mind that small volumes might contribute to a false-negative result. Falsenegative results are common in horses with severe osteoarthritis, and larger volumes of local anesthetic solution should be used. We routinely spray or wipe antiseptic solution over the injection site. After the examination a light bandage is applied over the injection sites from the metacarpophalangeal or metatarsophalangeal joint, distally. Initial reevaluation is done 5 to 10 minutes after injection. Additional evaluations may be necessary depending on the response during the initial time period. General practice is to have the horse walked in hand or with a rider after perineural or intrasynovial analgesia is administered, a procedure thought to hasten distribution of local anesthetic solution and potentially improve success. Excessive diffusion of local anesthetic solution is a potential drawback to this practice, particularly with techniques such as DIP or middle carpal analgesia (see the following discussion), although it would be a complication difficult to quantify. Another issue to consider when performing diagnostic analgesia is whether riding or driving a horse after blocks have been performed is safe. In general, riding on the flat or driving a horse at slow speed after any of the common blocks have been performed is safe. Stumbling or knuckling can be a concern after upper limb perineural techniques, such as the median and ulnar and fibular (peroneal) and tibial techniques. Common sense should prevail, however, with regard to the horse and rider negotiating fences or performing at high speed. Horses at risk for lameness from stress or incomplete fracture are candidates for imaging before evaluation at speed after diagnostic analgesic techniques have been performed. Moreover, horses suspected of having incomplete fractures but with negative or equivocal radiological findings may best be managed conservatively without use of analgesic techniques and should undergo either follow-up radiographic examination in 10 to 14 days or scintigraphic examination.

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PERINEURAL ANALGESIA IN THE FORELIMB Palmar Digital Analgesia Palmar digital analgesia (or palmar digital block) is the most common diagnostic analgesic procedure performed. The medial and lateral digital neurovascular bundles, consisting, in a dorsal to palmar direction, of the digital vein, artery, and nerve, course in an abaxial location to the digital flexor tendons. With the exception of small breeds or draft horses with remarkably long-haired pasterns (feathers), the palmar digital nerve is easily palpable between the proximal sesamoid bones and the cartilages of the foot. The palmar digital block can be performed with the horse in a standing position or with the limb held off the ground. We prefer the latter. If held by an assistant, the limb should be grasped in the midmetacarpal region, with the fetlock and digit hanging in neutral position. The palmar digital nerve is easily palpated in this extended position on the lateral aspect of the deep digital flexor tendon (DDFT). Alternatively, the clinician performing the block can hold the limb, a technique that requires practice. The clinician can stand facing backward with a hand grasping the midpastern region or can stand behind the limb and clutch the hoof between both legs. A 25-gauge, 1.6-cm needle is inserted subcutaneously, directly over the nerve, just proximal to the cartilages of the foot (Figure 10-5). One of us (LHB) directs the needle in a distal direction, whereas the other (MWR) directs the needle in a proximal direction to avoid deeper penetration or laceration of digital vessels if the horse withdraws the limb. Alternatively, a 22-gauge, 4-cm needle can be inserted on the palmar midline in the midpastern region, and local anesthetic solution is then infiltrated in a V-shaped pattern. This modification of the palmar digital block is quite difficult to perform in the hindlimb but when done in the forelimb provides maximal analgesia to the bulbs of the heel and minimizes the potential for depositing local anesthetic solution dorsal to the nerve. Loss of skin sensation in the midline between the bulbs of the heels should be assessed, because this area seems most recalcitrant to palmar digital analgesia. Deep pain is assessed using hoof testers. However, if skin sensation persists, it is still worth reevaluating lameness, because in some horses deep pain and lameness may be abolished despite the persistence of skin sensation. Traditionally the palmar digital block was felt consistently to desensitize only the palmar (plantar) one third to one half of the foot.21 However, in clinical practice, this block desensitizes 70% to 80% of the foot. Most of the DIP joint is affected, with the exception of the proximodorsal aspect. Horses with fractures of the extensor process of the distal phalanx or injury of a collateral ligament of the DIP joint may show partial improvement after palmar digital analgesia, however. Our clinical observations have been substantiated in a recent study. Setscrews were placed near the medial and lateral aspects of the toe to simulate pain from the sole. Lameness in these horses was abolished using palmar digital analgesia performed just proximal to the heel bulbs.22 Classically, most horses that responded positively to palmar digital analgesia were thought to have navicular syndrome, but this block desensitizes many lameness conditions within and outside the hoof capsule (Table 10-1).

This is an important and common misconception. Lameness in horses with proximal interphalangeal joint pain, midsagittal fracture of the proximal phalanx, or other conditions involving the fetlock joints can be abolished using palmar digital analgesia.7,23 Although using small volumes of local anesthetic solution and performing the block just above the cartilages of the foot may help to minimize the area of analgesia, these procedures do not prevent inadvertent diagnosis in some horses. Diffusion of local anesthetic solution is the most likely explanation, and even a small volume can readily spread in a proximal direction, but the normal anatomy of the digit prevents distal placement of local anesthetic solution (Figure 10-6). The concept that palmar digital analgesia abolishes lameness in an area considerably more than the palmar (plantar) one third of the foot appears to be difficult for many to accept. Although results of studies are widely published and this finding has been emphasized at international meetings, most veterinary students still graduate today armed with this common misconception. Diffusion of local anesthetic solution easily explains why lameness conditions in the proximal aspect of the pastern or fetlock regions are desensitized by palmar digital analgesia. But what about the innervation of the hoof itself? Skeptics should consider the anatomy of the palmar digital nerve. Most practitioners have severed the palmar digital nerve while performing neurectomy. Can the clinicians recall any instance of having identified a large dorsal branch, or for that matter, any branching of the nerve at all? The lack of nerve branches in the midpastern region is circumstantial evidence that important innervation to the structures located dorsally within the hoof capsule occurs farther proximally (ill-defined dorsal branches) or after the nerve courses deep to the cartilages of the foot. It makes little sense that ill-defined dorsal branches would innervate the dorsal two thirds of the foot, leaving the robust palmar digital nerve to innervate only the palmar one third. When carefully dissected the palmar digital nerves can be seen branching extensively deep to the cartilages of the foot, sending branches dorsally to innervate the dorsal portions of the foot. Accurately quantifying the contribution of the palmar digital nerve to the innervation of the foot or, for that matter, the exact percentage of structures desensitized by palmar digital analgesia may be impossible. Clinical experience will undoubtedly convince practitioners of the broad nature of palmar digital analgesia. Finally, it is imperative to develop expertise in diagnostic imaging of the entire digit, because the many lameness conditions affected by palmar digital analgesia require detective-like differential diagnostic skills.

Midpastern Ring Block

Traditionally the diagnostic blocks performed after palmar digital analgesia are the basisesamoid or abaxial sesamoid techniques. The basisesamoid block provides little additional information compared with palmar digital analgesia, unless, of course, the dorsal branch, originating from the digital nerve at the level of the proximal sesamoid bones, is blocked. If, however, the dorsal branch is blocked, then the basisesamoid block is in reality an abaxial sesamoid block. For this reason, we rarely perform the basisesamoid block. When performing the abaxial sesamoid

Lateral palmar vein, artery, and nerve

Dorsal branch of lateral palmar nerve

Lateral palmar vein, artery, and nerve

Dorsal branch of lateral palmar nerve

b

c Lateral palmar digital nerve

b

Lateral palmar digital nerve

a

a

A

B

Medial palmar digital nerve

Lateral palmar digital nerve

C Fig. 10-5  •  A, Palmarolateral view of the distal aspect of the limb showing site for needle penetration for palmar (plantar) digital analgesia (a). The clinician directs the needle as shown or in a proximal direction. The palmar (plantar) digital nerve is blocked more proximally at the level of the abaxial surface of the proximal sesamoid bone (b). At this level the palmar (plantar) digital nerves and dorsal branches are both blocked. B, Dorsolateral view of the distal aspect of the limb demonstrating needle positions for palmar (plantar) digital analgesia (a) with an additional dorsally directed subcutaneous ring block to desensitize the dorsal aspect of the pastern region and foot (b). A block at the base of the proximal sesamoid bone (c) likely desensitizes the palmar (plantar) digital nerves and dorsal branches of the digital nerve (note close association of both branches to the site of the block) and provides the same region of analgesia as does the palmar digital block with the dorsal ring, or the abaxial sesamoid block. C, Alternative technique used for the palmar digital nerve block. The clinician inserts the needle on the palmar midline and places a line of local anesthetic solution in a proximal dorsal direction to the level of each of the medial and lateral palmar nerves in an approximately V-shaped pattern. This technique confines local anesthetic solution to the palmar aspect of the limb. This blocking technique is difficult to perform in the hindlimb.

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TABLE 10-1 

Differential Diagnostic Analgesia of the Equine Foot DISEASE Navicular disease Synovitis DIP joint Osteoarthritis DIP joint Subchondral bone DIP joint P3 fracture (wing) P3 fracture (midsagittal) Extensor process fracture (P3) Pedal osteitis Subsolar abscess Solar pain (heel, quarter) Solar pain (toe) DDF tendonitis DDF enthesitis (P3 insertion) Sheared heel Quittor Laminitis (toe) Laminitis (quarter, heel) Toe crack Quarter crack, heel crack Distal sesamoidean desmitis PIP joint problem DFTS problem P2 Fracture P1 Fracture

PALMAR DIGITAL NERVE BLOCK

DISTAL INTERPHALANGEAL JOINT BLOCK

NAVICULAR BURSA BLOCK

+ + + + + ± ± + + + + + + + + — + — + ± ± ± ± ±

± + + ± + + + ± ± ± ± — ± — — — ± — ± — — — ± —

+ + + ± — — — ± ± ± + — — — — — — — — — — — — —

DDF, Deep digital flexor; DFTS, digital flexor tendon sheath; DIP, distal interphalangeal; P1, proximal phalanx; P2, middle phalanx; P3, distal phalanx; PIP, proximal interphalangeal.

technique in racehorses, or, for that matter, in any sport horse with a propensity to develop lameness of the metacarpophalangeal or metatarsophalangeal joints, the veterinarian runs the risk of an additional misdiagnosis. When local anesthetic solution is deposited in a location abaxial to the proximal sesamoid bones, pain from the metacarpophalangeal or metatarsophalangeal joints can be inadvertently blocked, explained most likely because of diffusion of local anesthetic solution, leading the clinician to assume the horse has a problem in the foot or digit, but in reality the pain originated from these joints. For these reasons, we prefer to use a blocking sequence as follows: palmar digital nerve, followed by a dorsally directed subcutaneous ring block, followed by the low palmar or plantar block. The midpastern ring block affects the dorsal branches of the digital nerves and desensitizes any remaining areas of the foot and pastern region that were not affected by palmar digital analgesia. In most horses this includes the dorsal 20% of the foot (dorsal laminar and extensor process regions of the distal phalanx) and the dorsal pastern region (dorsal aspects of the middle phalanx and proximal interphalangeal joint, and distal portions of the proximal phalanx). Although desirable, performing the dorsal ring block just above the cartilages of the foot usually is not possible. Instead the block is performed at the level of the midpastern region. A 20- to 22-gauge, 4-cm needle is used to deposit subcutaneously 10 to 12 mL of local anesthetic solution, beginning near the injection site used for palmar digital analgesia

over the lateral neurovascular bundle and continuing dorsally and medially, ending over the medial neurovascular bundle (see Figure 10-5). Resistance to needle advancement and injection of local anesthetic solution will invariably be encountered dorsally, if the block is done just proximal to the coronary band, because of the dense tissue (proximal interphalangeal joint capsule, extensor branches of the suspensory ligament, and extensor tendons). Performing the block in the midpastern region minimizes this problem and mitigates the potential for inadvertent penetration of the proximal interphalangeal joint.

Abaxial Sesamoid Block

Desensitizing the medial and lateral palmar nerves at the level of the proximal sesamoid bones is commonly referred to as the abaxial sesamoid block but may provide the same information as the basisesamoid block, if the dorsal branch of the palmar digital nerve is blocked. To avoid redundancy, we rarely perform the basisesamoid technique before progressing to the abaxial sesamoid block (see previous comments). A block done at this level essentially provides analgesia of the entire digit, because the block is performed at the level of or just proximal to the origin of the dorsal branch of the palmar digital nerve. Response to this block may vary, however. Some horses retain skin sensation in the dorsoproximal aspect of the pastern region. In others, pain arising from lesions involving the fetlock joint or periarticular tissues is abolished. In part, these phenomena can be explained by proximal diffusion



Fig. 10-6  •  Radiograph showing palmar digital analgesia performed with positive contrast material. The clinician performed palmar digital analgesia as far distal as possible, but the injection site is still at the level of the proximal interphalangeal joint, explaining why palmar digital analgesia desensitizes most of the foot and the pastern region in some horses.

of local anesthetic solution, affecting the palmar digital nerves proximal to the fetlock joint. Branches of the palmar digital nerves supplying the proximal sesamoid bones, the sesamoidean nerves, could easily be blocked using an analgesic technique in this abaxial position.24 One of the Editors (SJD) regularly performs palmar nerve blocks at the base of the proximal sesamoid bones as a first block if, on the basis of clinical examination, it is considered unlikely that the horse has foot-related pain and there is also no evidence of likely fetlock joint pain. The abaxial sesamoid block can be performed in the standing horse or with the limb held by the clinician or an assistant. The assistant grasps the foot, facing forward. The assistant should be warned that a fractious horse may kick backwards with the limb, so he or she should stand slightly to one side, outside the plane of the limb. The palmar digital nerve can easily be palpated over the rigid proximal sesamoid bones and in fact is in its most superficial position in this location. A 25-gauge, 1.6-cm needle is directed in a proximal or distal direction and typically 1 to 3 mL of local anesthetic solution are used for each of the medial and lateral injections. Deep pain is assessed by hard flexion of the interphalangeal joints. False-negative or delayed results can arise because of deposition of local anesthetic solution outside the fascia that surrounds the neurovascular bundle.8

Low Palmar Analgesia

Analgesia of the metacarpophalangeal joint region and distal aspect of the limb is induced using the low palmar

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block or low palmar analgesia (low four-point). This technique blocks the medial and lateral palmar nerves and the medial and lateral palmar metacarpal nerves. In the forelimb a subcutaneous, dorsally directed ring block and block of the dorsal branch of the ulnar nerve completely abolishes skin sensation. Disagreement exists about whether abolishing skin sensation is necessary when performing perineural techniques. Abolition of skin sensation independently from nerves contributing to deep pain sensation, as in the case of the low palmar technique, does not necessarily mean deep pain is abolished, which is particularly relevant when a nerve responsible for skin sensation is blocked. When using these techniques for diagnostic purposes, it may be best to avoid blocking nerves that contribute only skin sensation, thus minimizing the number of needle insertions For therapeutic interventions, however, these nerves need to be blocked. The low palmar block is performed at the level of the distal end (bell or button) of the second and fourth metacarpal bones (splint bones), with the limb in a standing position or held off the ground (Figure 10-7). A 20- or 22-gauge needle is used to inject 1.5 to 5 mL of local anesthetic solution at each injection site. To block the palmar metacarpal nerves, the needle is inserted perpendicular to the skin, just distal to the end of the splint bones, to a depth of 1 to 2 cm. It is important to deposit local anesthetic solution deep in the injection site, rather than simply in a subcutaneous location. While local anesthetic solution is continuously injected, the needle is slowly withdrawn, leaving a visible bleb in the subcutaneous space. To block the medial and lateral palmar nerves, the needle is inserted subcutaneously, in the palmar aspect of the space between the suspensory ligament and DDFT at the level of or slightly more proximal to the distal end of the splint bone. To improve the accuracy of the injection, using a fan-shaped injection technique is helpful. If the digital flexor tendon sheath (DFTS) is distended, the injections must be performed more proximally. Inadvertent penetration of the DFTS is possible even if it is not distended, so careful skin preparation is mandatory. To complete this block, local anesthetic solution is placed in the subcutaneous tissues from the bleb at the distal end of the splint bone to the dorsal midline. One of the Editors (SJD) does not do this last step. An alternative technique to abolish pain associated with maladaptive or nonadaptive bone remodeling or other causes of subchondral bone pain of the distal aspect of the McIII is to block the lateral and medial palmar metacarpal nerves separately from the lateral and medial palmar nerves. In some horses suspected of having this injury, use of abbreviated low palmar analgesia will avoid additional injections of local anesthetic solution. With this technique the lateral or medial palmar metacarpal nerve, or both, can be blocked individually or together, and the horse’s gait assessed. In many horses with this cause of lameness, contralateral forelimb lameness will then be seen. If lameness does not abate, the clinician then completes low palmar analgesia using the technique described previously (see the following discussion). Alternatively, some clinicians prefer to use a longer needle first to deposit local anesthetic solution over the palmar metacarpal (metatarsal) nerves. The needle is then pushed subcutaneously to deposit local anesthetic solution over the palmar nerves (see Figure 10-7). When this

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DDFT SDFT

c b

a b

Common and lateral digital extensor tendons

SL

a

A

SL

B Fig. 10-7  •  A, This lateral view shows needles positioned for a low palmar (plantar) nerve block. The clinician inserts a needle (a) just distal to the distal aspect of the fourth metacarpal or metatarsal bone and directs it axially to block the lateral palmar (plantar) metacarpal (metatarsal) nerve. The clinician then inserts a needle (b) between the suspensory ligament (SL) and deep digital flexor tendon (DDFT) to block the lateral palmar (plantar) nerve. The clinician repeats the two injections on the medial side. A subcutaneous ring block from the first injection site around to the dorsal midline (c) completely abolishes skin sensation. B, Transverse view of the distal left metacarpal region demonstrating an alternative technique for low palmar (plantar) analgesia. The clinician inserts a needle (a) in a lateralto-medial direction between the DDFT and the SL to block the lateral and medial palmar (plantar) nerves. The palmar (plantar) metacarpal (metatarsal) nerves are blocked as depicted in A (not shown in this diagram), which also shows the subcutaneous ring block. The clinician inserts a needle (b) in a lateral-to-medial direction dorsal to the digital extensor tendons to block the dorsal metatarsal nerves of the hindlimb.

modification is performed, incompletely blocking the palmar metacarpal (metatarsal) nerves or lacerating the digital vessels is possible. The lateral and medial palmar nerves can be blocked using only the lateral injection site by advancing the needle in a medial direction, palmar to the DDFT. Although each of these modifications may theoretically decrease the number of injections needed to perform this technique, they have the disadvantages of potential hemorrhage and incomplete analgesia.

High Palmar Block

To provide analgesia to the metacarpal region, the high palmar block (high four-point, subcarpal block) is the most common technique, but a modified block (lateral palmar or Wheat block) can be performed. Inadvertent penetration of the carpometacarpal joint is a potential complication with the high palmar block. A similar complication can occur in the hindlimb but is less frequent (see the following discussion). Inadvertent penetration of the carpometa­ carpal joint occurred in 17% of specimens, in which a conventional high palmar block was performed, because of extensive distopalmar outpouchings (Figures 10-8 and 109). However, when the high palmar block was performed within 2.5 cm of the carpometacarpal joint, inadvertent penetration of this joint occurred in 67% of specimens. The carpometacarpal joint always communicates with the

middle carpal joint, and therefore penetration of the carpometacarpal joint during high palmar analgesia would lead the clinician to diagnose a metacarpal problem, when in reality the authentic lameness condition exists in the carpus. Moving the injection site in a distal direction decreases the possibility of entering the carpometacarpal joint but also narrows the scope of the technique and may result in a false-negative response in a horse with proximal suspensory desmitis. Two ways around this likely complication are these: first, the clinician could perform middle carpal analgesia before performing high palmar analgesia; second, the clinician could perform a lateral palmar block in lieu of the conventional high palmar technique. In an experimental study, the carpal joints were unlikely to be entered inadvertently during performance of the lateral palmar block, although in every specimen, local anesthetic solution would have entered the carpal canal.25 Unless the clinician is familiar with the lateral palmar block, the most straightforward approach to reduce the possibility of misdiagnosis in this region is to perform middle carpal analgesia before proceeding to the high palmar block. When local anesthetic solution is placed in the middle carpal joint, not only is the carpometacarpal joint blocked, but also the possibility exists of providing local analgesia to the proximal palmar metacarpal region. With this approach, abolishing pain associated with proximal suspensory attachment

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mc

cmc

Fig. 10-8  •  Positive contrast arthrogram of the middle carpal (mc) and carpometacarpal (cmc) joints (dorsal is to the right). Contrast material injected into the middle carpal joint flows freely distally into the carpometacarpal joint and fills the extensive distopalmar outpouchings of the joint (arrow).

A

B

Fig. 10-9  •  Liquid acrylic injected into the middle carpal joint and allowed to harden created this specimen showing the lateral (A) and medial (B) distopalmar outpouchings of the carpometacarpal joint. Secondary fingerlike outpouchings ramify in the proximal palmar metacarpal region.

Fig. 10-10  •  Transverse section of the proximal metacarpal region just distal to the carpometacarpal joint after latex injection into the middle carpal joint showing primary and secondary distopalmar outpouchings of the carpometacarpal joint (dark areas, arrows) interdigitating with the proximal aspect of the suspensory ligament (dorsal is up; lateral is left). This anatomical arrangement explains inadvertent analgesia of the carpus and proximal palmar metacarpal region during high palmar and middle carpal analgesia, respectively. McIII, Third metacarpal bone.

avulsion injury (desmitis, fracture), stress remodeling, and longitudinal fracture is possible (see Chapter 37). The palmar metacarpal nerves and suspensory branches from the lateral palmar nerve are closely associated with the distopalmar outpouchings of the carpometacarpal joint, and diffusion of local anesthetic solution from this area could explain in part this clinical finding (Figure 10-10). It is important for the clinician to understand that interpretation of analgesic techniques in the proximal palmar metacarpal region or carpus can be somewhat complex. Correct diagnosis is always the key, and comprehensive evaluation using multiple imaging modalities is a must in differentiating lameness in this region. From the clinical perspective, one is more likely to assume incorrectly that one is dealing with a carpal problem when the authentic lameness condition resides in the proximal palmar metacarpal region than vice versa. Numerous techniques are used to perform high palmar analgesia; some provide partial and others provide complete analgesia to the metacarpal region. For complete analgesia, blocking the following nerves is necessary: the medial and lateral palmar nerves, the medial and lateral palmar metacarpal nerves, the suspensory branches, and nerves providing skin sensation along the dorsum (dorsal branch of ulnar nerve and musculocutaneous nerve). To block these nerves effectively, one must use a site close to the carpometacarpal joint, at the level where the splint bones begin to taper (Figure 10-11). If the block is done at a lower level, the region of the suspensory attachment will be missed. A 20or 22-gauge needle at least 2.5 cm long is necessary to reach the palmar metacarpal nerves in this location. The needle is inserted axial to the splint bones just abaxial to the suspensory ligament and then guided to the palmar

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Lateral palmar metacarpal nerve

Medial palmar nerve

a b Fig. 10-11  •  Transverse view of the left metacarpal region showing the technique for high palmar analgesia. The clinician inserts a needle (a) axial to each second and fourth metacarpal bone and uses two separate injections (b) to block the medial and lateral palmar nerves. The location of the high palmar technique appears in the lateral view (inset).

cortex of the McIII. Five milliliters of local anesthetic solution are deposited, first deep within the tissues, and continued as the needle is withdrawn, ending with a bleb in the subcutaneous tissues. To block the medial and lateral palmar nerves between the suspensory ligament and DDFT, a smaller-gauge needle can be used to deposit 3 to 5 mL of local anesthetic solution at each of two sites. To complete this block, a circumferential subcutaneous ring block is performed to abolish skin sensation dorsally. Alternatively, the subcutaneous nerves can be blocked on either side of the common digital extensor (CDE) tendon, but small zones of sensation may persist when this technique is used. It is only necessary to complete the dorsal portion of this block to provide complete analgesia when performing procedures in the dorsal metacarpal region, such as laceration repair or standing osteostixis. A modification of the high palmar block is performed by locally infiltrating the suspensory origin from a lateral injection site in a fan-shaped pattern. This procedure, along with one specifically to block the medial and lateral palmar metacarpal nerves, improves specificity of this complex block, because pain from only a limited number of structures is eliminated. The medial and lateral palmar nerves can also be blocked from a single lateral injection site. One of the Editors (SJD) regularly blocks just the palmar metacarpal nerves (using only 2 to 3 mL of local anesthetic solution per site) and only adds perineural analgesia of the palmar nerves if the first block is negative, in order to facilitate differentiation of suspensory ligament or McIII pain from pain arising from the more palmar soft tissue structures. A dorsal ring block is never used.

Lateral Palmar Block

An alternative method of providing analgesia to the metacarpal region is to perform what is known as the lateral

palmar (high two-point) or Wheat block.26 For complete analgesia, however, combining this block with an independent injection over the medial palmar nerve and with a dorsal subcutaneous ring block is necessary. Originally proposed as an alternative method for analgesia of the suspensory ligament origin, this technique involves blocking the lateral palmar nerve just distal to the accessory carpal bone (Figure 10-12). The lateral palmar nerve is formed as the median and deep ulnar nerves join, proximal to the accessory carpal bone (see Figure 10-12).27 At the level of the block, just distal to the accessory carpal bone, the lateral palmar nerve is blocked before it branches to form the medial and lateral palmar metacarpal nerves and the suspensory branches and continues distally (see Figure 10-12). The high two-point block is completed with the separate but concurrent block of the medial palmar nerve. This technique has at least three advantages compared with conventional high palmar analgesia. Inadvertently penetrating the distopalmar outpouchings of the carpometacarpal joint is virtually impossible, although local anesthetic solution will likely enter the carpal canal.25 Lateral palmar analgesia requires fewer needle penetrations than does conventional high palmar analgesia. Finally, only a small volume of local anesthetic solution is necessary to desensitize a number of nerves and the origin of the suspensory ligament. Pain associated with the carpal canal is abolished, however, and can be present without palpable effusion. The lateral palmar block can be performed in the standing position or with the limb held off the ground, with the carpus in 90 degrees of flexion. The nerve cannot be palpated because it courses in the accessorial-metacarpal ligament, dense connective tissue distal to the accessory carpal bone. A 25-gauge, 1.6-cm needle is inserted to the hub, perpendicular to the skin, just distal to the accessory carpal bone, and 5 mL of local anesthetic solution are deposited within this dense tissue. Injection can be difficult to perform, and breaking the seal between the needle and syringe is common, so a screw-type hub should be used. The medial palmar nerve is then blocked as described previously. If desired, a dorsal, circumferential subcutaneous ring block provides complete analgesia to the dorsum. An alternative technique for lateral palmar nerve block has recently been described.28 The primary advantage of this technique is that it mitigates the risk of inadvertent penetration of the carpal synovial sheath (carpal canal). The block is performed with the limb in extension. The primary landmark is a palpable groove in the flexor retinaculum just dorsal to its insertion on the palmaromedial aspect of the accessory carpal bone. A 1.5-cm, 25-gauge needle is inserted in the distal third of the groove in a mediolateral direction, and when contact is made with the medial surface of the accessory carpal bone, local anesthetic solution is injected. However, it is quite easy for the needle to hit the nerve, which results in the horse striking out, and a difficult horse may become even more fractious to block.

Median, Ulnar, and Medial Cutaneous Antebrachial Blocks

Analgesia of the distal aspect of the antebrachium and carpus can be induced by blocking the median, ulnar,

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Ulnar nerve

Ulnar nerve

Palmar branch of ulnar nerve Lateral palmar nerve Lateral palmar metacarpal nerve

Median nerve

Median nerve

Medial palmar nerve

Deep branch of lateral palmar nerve Branches to the suspensory ligament

Ulnar nerve Lateral palmar nerve Medial palmar nerve

Dorsal branch of ulnar nerve

Deep branch of lateral palmar nerve

Lateral palmar nerve

A

115

Lateral and medial palmar metacarpal nerves

B Fig. 10-12  •  A, This diagram of the left carpus in a flexed position shows the location of the lateral palmar nerve block and parent nerves (inset) contributing to the origin of the lateral palmar and other important nerves. B, Palmar view of the limb showing nerves in situ and the site for needle penetration for lateral palmar nerve block.

and medial cutaneous antebrachial (musculocutaneous) nerves.21 Because the last nerve supplies only skin sensation, for diagnostic purposes it does not need to be included in the technique. In our practices these blocks are most commonly performed to facilitate lavage of the carpal joints or carpal canal or to perform regional limb perfusion of antibiotics in standing horses. We generally default to intrasynovial analgesia in these structures, however. However, one of us (MWR) has recently evaluated several horses with subchondral bone pain in the middle carpal joint in which intraarticular carpal analgesia failed to abolish clinical signs of pain. Lameness was abolished using the median and ulnar blocks. One Editor (SJD) finds these blocks extremely valuable in horses that do not respond to subcarpal or intraarticular carpal analgesia and employs median and ulnar blocks routinely. Although the median and ulnar blocks remain infrequently used in the United States, perhaps they should be considered routine. Median, ulnar, and medial cutaneous antebrachial nerve blocks are useful in diagnosing subchondral carpal bone pain or lameness involving the carpal canal. Although the prevalence of lameness in the distal aspect of the antebrachium is low, these blocks can be used to diagnose distal radial bone cysts or enthesitis at the origin of the accessory ligament of the superficial digital flexor tendon (SDFT) (superior check ligament). These blocks can be used to eliminate the entire distal aspect of the limb as a potential source of pain. Alternatively, these blocks can be used alone to eliminate pain distal to the injection site, or the median and ulnar nerves can be blocked independently to improve specificity of the technique. The ulnar nerve is blocked about 10 cm proximal to the accessory carpal bone on the caudal aspect of the antebrachium (Figure 10-13). A 20- or 22-gauge, 4-cm needle is

inserted to the hub, perpendicular to the skin, in the groove between the flexor carpi ulnaris and the ulnaris lateralis muscles. Needle contact with the ulnar nerve may cause the horse to strike forward.5 Ten milliliters of local anesthetic solution are injected as the needle is slowly withdrawn. Skin sensitivity along the lateral aspect of the limb from the carpus to the metacarpophalangeal joint will be eliminated.21 The median nerve is blocked 5 cm distal to the cubital (elbow) joint on the medial aspect of the antebrachium. At this level, the nerve lies along the caudal aspect of the radius, just cranial to the flexor carpi radialis muscle. A 20- or 22-gauge, 4-cm needle is inserted into the hub, in a lateral direction, along the caudal aspect of the radius, just distal to the superficial pectoral muscle, and 10 mL of local anesthetic solution are used (see Figure 10-13). Rarely in large horses, a 9-cm (3 1 2-inch) spinal needle may be necessary to reach the median nerve. Often the needle hits the median nerve, a useful indicator that the tip is in the proper location.5 In any event the needle should be kept close to or against the caudal cortex of the radius to avoid inadvertent puncture of the median artery or vein, which lies caudal to the nerve.21,27 However, inadvertent puncture determines that the needle is close to the correct site and is highly unlikely to cause any adverse reaction. To facilitate these deep injections, the skin can be first desensitized by using a small volume of local anesthetic solution. A more distal injection site for the median nerve may eliminate the possibility of inadvertently eliminating elbow joint pain using the suggested approach.5 Finally (for therapeutic applications), to block the cranial and caudal branches of the medial cutaneous antebrachial (musculocutaneous) nerve, 3 mL of local anesthetic solution are injected, subcutaneously, on the cranial

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Flexor carpi ulnaris muscle

b

Ulnar nerve

Extensor carpi radialis

Median nerve

a

Cephalic and accessory cephalic vein

Musculocutaneous nerve

b

Ulnaris lateralis muscle

Median nerve Flexor carpi ulnaris muscle

Ulnar nerve

A

Lacertus fibrosus

a

Radius

B

Fig. 10-13  •  A, This caudal view of the left antebrachium shows the sites of needle insertion for the median and ulnar nerve blocks. A needle placed between the ulnaris lateralis and flexor carpi ulnaris muscles (a), about 10 cm proximal to the accessory carpal bone, blocks the ulnar nerve. A needle inserted along the caudal aspect of the radius about 10 cm distal to the elbow joint (b) blocks the median nerve. The inset shows the orientation between the radius, median artery, vein, and nerve at the site of needle insertion (b) and shows the orientation of the needle for the ulnar nerve block (a), which is performed distally. B, This medial view of the proximal left antebrachium shows the technique for a musculocutaneous nerve block. The nerve is blocked as it crosses the lacertus fibrosus on the cranial aspect of the proximal antebrachium. This block abolishes skin sensation on the medial and dorsal aspects of the antebrachium.

and caudal aspect of the accessory cephalic and cephalic veins, about halfway between the carpus and elbow (see Figure 10-13).21 Alternatively, this nerve can be blocked before it branches, as it courses across the lacertus fibrosus. At this location, the nerve is easily palpable in most horses. A third method to completely abolish skin sensation is using a circumferential subcutaneous ring block, a technique that can effectively block all four cutaneous antebrachial nerves but requires a large volume of local anesthetic solution.

INTRAARTICULAR ANALGESIA IN THE FORELIMB Distal Interphalangeal Joint

The assumption is that analgesia of the DIP joint is specific for intraarticular pain, but clinical experience and the results of recent clinical and anatomical investigations have convinced us otherwise (see Figure 10-1). Of great clinical interest is the comparative accuracy of analgesia of the DIP joint and navicular (podotrochlear) bursa in the diagnosis of navicular syndrome. Overall, analgesia of the navicular bursa is likely the most specific technique to diagnose navicular syndrome. However, results of two studies suggest that this block may not be as specific as once thought (see the section on analgesia of the podotrochlear bursa).29,30 Analgesia of the DIP joint lacks specificity for intraarticular pain and in fact can eliminate pain associated with many conditions of the foot.29-32 For instance, when high-performance liquid chromatography was used to study the effects of 8 mL of mepivacaine injected into the DIP joint, there was local anesthetic solution in the synovium of the navicular bursa in all horses and in the

medullary cavity of the navicular bones in 40% of horses.33 Similarly, a recent in vitro study showed that 15 minutes after injection of 5 mL of 2% mepivacaine into either the navicular bursa or the DIP joint, mepivacaine was detected in the alternate (uninjected) synovial structure in all specimens. In 48% of navicular bursae after DIP joint injection, and in 44% of DIP joints after navicular bursa injection, mepivacaine was present in clinically effective (analgesic) concentrations (>100 to 300 mg/L).34 Anatomical studies showed that nociceptive neurofibers are present in the dorsal and palmar aspects of the collateral sesamoidean ligaments, within the distal sesamoidean impar ligament, and directly innervating the navicular bone, in the periarticular connective tissues of the DIP joint and proximal intramedullary portions of the distal phalanx.35,36 The close anatomical relationship among all of these structures and the palmar digital neurovascular bundles to the DIP joint capsule makes them susceptible to desensitization by local anesthetic solution injected into the DIP joint.36 In a study using a setscrew model to create solar pain at the toe, DIP intraarticular analgesia abolished lameness, leading to the conclusion that pain in distant sites can be abolished using this technique.22 Therefore a positive response to DIP intraarticular analgesia could mean lameness is caused by an articular problem, navicular syndrome, or, for that matter, solar pain. Close juxtaposition between the palmar synovial extensions of the DIP joint and digital nerves at this level was theorized as the reason that these nerves were blocked, secondary to diffusion of local anesthetic solution from the joint.22 Therefore a protocol to examine a lame horse no longer than 5 minutes after intraarticular analgesia of the DIP joint may theoretically

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a b

a Dorsal pouch of DIP joint

b

CDET

c Palmar pouch of DIP joint

c

Fig. 10-14  •  Lateral view of the foot showing our preferred approach for arthrocentesis of the digital interphalangeal joint using a dorsal midline needle insertion site (a) and directing the needle slightly distally through the common (long) digital extensor tendon. Alternatively, the clinician approaches the digital interphalangeal joint using a site medial or lateral to the extensor tendon (b). The top inset shows the needle positions from the dorsal aspect. The clinician may use a palmar (plantar) approach by positioning the needle between the distal palmar (plantar) border of the middle phalanx and a palpable notch in the proximal border of the cartilage of the foot. The clinician directs the needle (c) in a palmaroproximolateral to dorsodistomedial direction. The lower inset shows the notch into which the needle is inserted. CDET, Common (long) digital extensor tendon; DIP, distal interphalangeal.

minimize diffusion and improve accuracy. However, in one of the Editor’s (SJD) experience, pain associated with the navicular bone, navicular bursa, or DDFT has frequently been substantially improved within 5 minutes of injection of the DIP joint. Because diffusion of local anesthetic solution may be hastened by moving the horse, some clinicians prefer the horse to stand until the results of the block are evaluated.5 Traditionally, arthrocentesis of the DIP joint has been performed in the dorsal pouch, either medial or lateral to the CDE tendon. A 20-gauge, 2.5- to 4-cm needle is inserted about 1.5 cm proximal to the coronary band, abaxial to the CDE tendon, and directed in a distal and axial direction (Figure 10-14). An easier approach, however, is to insert the needle, angled just slightly distal from horizontal, on the dorsal midline, through the CDE. Synovial fluid is consistently obtained using this approach. One of the Editors (SJD) angles the needle more vertically, inserting it in the palpable dip in the distal dorsal aspect of the pastern. For the dorsal aspect of the DIP joint to be opened up, the limb should be positioned slightly ahead of the contralateral limb, and the horse should be in a standing position. Five to 10 mL of local anesthetic solution have been used traditionally, but a maximum of 6 mL may prevent leakage from the joint. Use of a lower volume of local anesthetic solution may also improve the specificity of the block, as was shown in a similar study using setscrews to create solar pain. Decreasing the volume of local anesthetic solution in the DIP joint from 10 mL to 6 mL resulted in a significant reduction in lameness caused by pain at the dorsal margin of the sole, but not at the angles of the sole.37 The horse is examined after 5 minutes. Alternatively, a lateral approach to the DIP joint can be used (see Figure 10-14). Landmarks include the distal palmar border of the middle phalanx dorsally and the

palpable notch in the proximal border of the lateral cartilage of the foot distally. A 4-cm needle is inserted laterally and directed in a dorsodistomedial direction. This technique, however, is less reliable than the dorsal approach, because contrast material entered exclusively the DIP joint in only 13 of 20 specimens and in 7 specimens inadvertently entered the navicular bursa or DFTS.38

Proximal Interphalangeal Joint

Arthrocentesis of the proximal interphalangeal joint is most commonly performed in the dorsal pouch. Effusion is rarely present even in horses with severe lameness, a situation that makes arthrocentesis challenging. The injection site is just lateral (or medial) to the CDE tendon at a level of or just distal to the distal, palmar process of the proximal phalanx, located and easily palpable on the distopalmar aspect of this bone. With the horse in the standing position, a 20-gauge, 2.5-cm needle is directed slightly distally and medially (using the dorsolateral approach) and inserted until articular cartilage is encountered (Figure 10-15). Although a desirable sign, synovial fluid appearing in the hub of the needle is an unusual occurrence. Local anesthetic solution, 5 to 10 mL, is injected, and the horse is examined after 5 minutes. An alternative approach that one author (MWR) finds much easier to perform is approaching the proximal palmar pouch of the proximal interphalangeal joint from the lateral aspect. The injection location is a V-shaped notch, located dorsal to the neurovascular bundle and between the distal palmar process of the proximal phalanx and the insertion of the lateral branch of the SDFT (see Figure 10-15). The limb is held off the ground with the digit in flexion, and a 2.5- or 4-cm needle is directed distomedially (and slightly dorsally) at an angle of about 30 degrees from the transverse plane until fluid is collected (generally at a

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118

Lateral palmar process CDET

Palmar recess of PIP joint

Dorsal pouch of PIP joint

Joint capsule

A

B Fig. 10-15  •  A, Dorsolateral view of the digit showing the site for arthrocentesis of the dorsal pouch of the proximal interphalangeal joint. The clinician inserts the needle just abaxial to the common digital extensor tendon at a site level with the palpable distal palmar (plantar) process of the proximal phalanx. B, Flexed lateral view of the digit indicating the site for arthrocentesis of the palmar (plantar) aspect of the proximal interphalangeal joint. The clinician inserts the needle into the V-shaped notch formed by the distal palmar (plantar) aspect of the proximal phalanx dorsally, the bony eminence associated with the attachment of the lateral collateral ligament to the distal aspect of the proximal phalanx and proximal aspect of the middle phalanx distally, and the insertion of the lateral branch of the superficial digital flexor tendon palmarodistally (plantarodistally). The clinician directs the needle distomedially (in a slightly dorsal direction) at an angle of about 30 degrees from the transverse plane until fluid appears. CDET, Common (long) digital extensor tendon; PIP, proximal interphalangeal.

depth of 2 to 3 cm).39 Advantages of this compared with the dorsal approach include less needle manipulation, a larger injection volume, and more frequent recovery of synovial fluid. The technique is difficult to perform with the limb in an extended weight-bearing position, because the palmar or plantar aspect of the proximal interphalangeal joint is compressed. Furthermore, diffusion of local anesthetic solution into palmar soft tissue structures can confound interpretation of results.5

Metacarpophalangeal Joint

Four sites commonly used for arthrocentesis of the metacarpophalangeal joint include the dorsal, proximopalmar, and distopalmar sites and the approach through the collateral ligament of the proximal sesamoid bone. The two most commonly used, the dorsal and proximopalmar sites, have potential disadvantages compared with the less commonly used sites. The dorsal pouch can be prominent in horses with effusion, but inadvertently stabbing articular cartilage repeatedly is common when this approach is used. The proximopalmar pouch or recess is large and easily identified, but prominent synovial villi often occlude the needle end, complicating retrieval of synovial fluid, even in horses with severe effusion. Hemorrhage associated with large intracapsular vessels is also a common complication with the proximopalmar approach. The palmar pouch is located dorsal to the suspensory branch, palmar to the McIII, proximal to the collateral sesamoidean ligament, and distal to the bell of the splint bone (Figure 10-16).

Fig. 10-16  •  Positive contrast arthrogram of the metacarpophalangeal joint showing the extensive nature of the palmar pouch that extends proximally to the level of the distal end of the splint bones. The distopalmar outpouchings are reliable sites for retrieval of synovial fluid and injection.

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b a Collateral sesamoidean ligament Proximal palmar process of proximal c phalanx

d Joint capsule

B

a

Suspensory ligament

A

Palmar annular ligament

Distal digital annular ligament

Proximal digital annular ligament

b C Fig. 10-17  •  A, Palmarolateral (plantarolateral) view of the left metacarpophalangeal (metatarsophalangeal) joint and digit showing the sites for arthrocentesis of the proximal palmar (plantar) pouch (a), the dorsal pouch (b), the distal palmar (plantar) pouch (c), and the palmar (plantar) pouch through the collateral ligament of the proximal sesamoid bone (d). B, Our preferred site for metacarpophalangeal (metatarsophalangeal) joint arthrocentesis, the distal palmar (plantar) approach, using a site just proximal to the lateral palmar (plantar) process of the proximal phalanx, is easily located in the standing or flexed position. C, Palmarolateral (plantarolateral) view of the digit indicating sites for synoviocentesis of the proximal (a) and distal (b) aspects of the digital flexor tendon sheath. Proximally, the clinician inserts the needle proximal to the palmar (plantar) annular ligament, and distally inserts the needle on the palmar (plantar) midline into an outpouching of the digital flexor tendon sheath between the proximal and distal digital annular ligaments.

Arthrocentesis using the proximopalmar approach can be performed with the limb in the standing position or being held. An 18- to 22-gauge, 2.5- to 4-cm needle is inserted in the center of the pouch and directed slightly distally in the frontal plane until synovial fluid is recovered (Figure 10-17). It may be necessary to aspirate synovial fluid if the joint capsule is not distended. Dorsally, arthrocentesis is performed medial or lateral to the CDE tendon (see Figure 10-17). With the limb in a standing or flexed position, the clinician can insert a needle in the distal aspect of the palmar pouch, through

the collateral sesamoidean ligament, a less common but effective approach for arthrocentesis of the metacarpophalangeal joint. The technique is more easily performed with the joint held in flexion. This approach for arthrocentesis was shown to be associated with less subcutaneous and synovial inflammation than was the proximopalmar approach40 and is the technique routinely used by one of the Editors (SJD). Under most circumstances we prefer to perform arthrocentesis of the metacarpophalangeal joint using the distopalmar approach. The injection site is in a small but

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PART I  Diagnosis of Lameness

Carpal Joints

reliable recess bounded by a triad of structures. Just proximal to the readily palpable proximal, palmar process of the proximal phalanx is a distinct depression. The dorsal aspect of the proximal sesamoid bone and the palmar condyle of the McIII complete the triad but are not readily palpable. The injection site is dorsal to the neurovascular bundle. Synovial fluid is consistently retrieved because the injection site is in the most distal aspect of the joint, and hemorrhage is rare. A large volume of fluid can be collected, if desired, because this area is devoid of the large synovial villi that complicate the proximopalmar approach. With the horse in a standing position, a 20-gauge, 2.5-cm needle is inserted, parallel to the ground, in a dorsomedial direction until fluid is obtained (see Figure 10-17). The needle can be advanced to the hub, but the joint is quite superficial in this location. This technique can also readily be performed with the limb being held in a flexed position. Ten mL of local anesthetic solution are injected, and the horse is reexamined in 5 to 10 minutes. In horses with subchondral bone pain, additional time may be necessary, but perineural analgesia may be necessary to abolish lameness in these horses. Diffusion of local anesthetic solution may account for partial or complete improvement in lameness in horses with suspensory branch desmitis, sesamoiditis, or injury of the straight, cruciate, or oblique sesamoidean ligaments. Therefore timely evaluation of horses after metacarpophalangeal analgesia is necessary.

Arthrocentesis of the middle carpal or antebrachiocarpal joints is one of the easiest and most straightforward of all joint injection techniques. With the carpus in flexion, injection sites are easily identified, and large portals exist through which to access the joints. Portals can be found either medial to the extensor carpi radialis (ECR) tendon or between the ECR and the CDE tendons (Figure 10-18). The middle carpal and carpometacarpal joints always communicate, but a communication between the middle carpal and antebrachiocarpal joints rarely exists. A communication between the middle carpal joint and carpal sheath only rarely is encountered clinically, but was not seen in a study using cadaver limbs. Analgesia of the middle carpal and antebrachiocarpal joints should be performed separately to differentiate lameness between these independent cavities. However, even though gross anatomic communications rarely exist between these joints, a recent in vitro study revealed the potential for diffusion of mepivacaine from one joint to the other by 15 minutes after either was injected with 10 mL of 2% mepivacaine. In only a small percentage were the concentrations of mepivacaine in each joint at levels thought to produce clinical analgesia. How this translates to the live horse also remains unknown. Nonetheless, the clinician is reminded of the importance of prompt reevaluation to minimize misinterpretation of the results, but also to keep an open mind if results of diagnostic imaging do not seem compatible with the results

a ECRT

CDET

c b

b

Carpal sheath

a A

a

d

c

B Fig. 10-18  •  A, Dorsal view of the left carpus in a flexed position showing the sites for arthrocentesis of the middle carpal (a) and antebrachiocarpal (b) joints. Needles are usually positioned between the extensor carpi radialis and common digital extensor tendons (as shown), but sites for injection of both joint cavities located medial to the extensor carpi radialis tendon can be used. B, Lateral view of the left carpus demonstrating sites for arthrocentesis of the proximal palmar pouch of the antebrachiocarpal joint (a), the palmarolateral pouch of the middle carpal joint (b), and the proximal (c) and distal (d) pouches of the distended carpal sheath. The inset shows the relative needle positions to enter the palmar pouch of the antebrachiocarpal joint and the carpal sheath. CDET, Common (long) digital extensor tendon; ECRT, extensor carpi radialis tendon.

of diagnostic analgesia.34 Distopalmar outpouchings of the carpometacarpal joint complicate interpretation of analgesic techniques, because these extend a mean distance of 2.5 cm distal to the carpometacarpal articulation and are closely associated with the suspensory ligament origin and the palmar metacarpal nerves (see Figures 10-8 to 10-10).41 Careful differential analgesic techniques and comprehensive imaging are necessary for accurate diagnosis of lameness in the carpal and proximal metacarpal regions. Typically, a 20-gauge, 2.5-cm needle is used to inject 5 to 10 mL of local anesthetic solution into the middle carpal and antebrachiocarpal joints. If the skin can be prepared aseptically on the dorsal aspect, the injections are most commonly performed with the joint in 90 to 120 degrees of flexion. The clinician can maintain flexion, but having an assistant hold the limb securely is easier. If the dorsal aspect of the carpus cannot be prepared aseptically, as occurs commonly in racehorses with chemically induced dermatitis (scurf), or if an additional site is needed for thorough lavage, the palmarolateral pouches of the middle carpal and antebrachiocarpal joints can be used. The palmar pouch of the antebrachiocarpal joint is bounded by the lateral digital extensor tendon dorsally and the ulnaris lateralis tendon palmarly. In horses with substantial effusion, this pouch is easily identified but must be differentiated from the lateral outpouching of the carpal sheath. Arthrocentesis can be performed either proximally or distally in the palmar pouch (see Figure 10-18). The distal injection site is located in a shallow recess between the distal lateral radius (ulna) and the ulnar carpal bone, just distal to the V-shaped convergence of the lateral digital extensor and ulnaris lateralis tendons. With the horse in a standing position, a 20-gauge, 2.5-cm needle is inserted perpendicular to the skin and advanced until synovial fluid is recovered. The palmar pouch of the middle carpal joint is similarly accessed in a shallow depression between the ulnar and fourth carpal bones, located 2 to 2.5 cm distal to the recess palpated to access the antebrachiocarpal joint in the palmar aspect (see Figure 10-18). The shallow depression in the middle carpal joint is difficult to palpate, but in horses with severe effusion an outpouching of the joint is palpable. This approach is undertaken with the limb in a standing position, decreases the potential for iatrogenic cartilage injury, and is less dangerous to the clinician because the procedure is performed on the side rather than in front of the limb.42 The injection is more difficult and less commonly used, however.

Cubital (Elbow) Joint

Two sites are used for arthrocentesis of the elbow joint. The cranial pouch is accessed at the level of the radiohumeral articulation, just cranial to the lateral collateral ligament. The lateral collateral ligament courses between the palpable lateral tuberosity of the radius and the lateral epicondyle of the humerus (Figure 10-19). An 18- or 20-gauge, 6- to 9-cm needle is directed medially and slightly caudally to a depth of 5 to 6 cm, beginning in the adult horse, about 3.5 cm proximal to the lateral tuberosity of the radius and 2.5 cm cranial to the lateral collateral ligament.19 To account for differences in horse size, the injection site is generally located two thirds of the distance between the humeral epicondyle and the lateral tuberosity of the radius.

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This block may be more easily performed closer to the lateral collateral ligament, and at this site the joint is penetrated in a more superficial location.5 Before injection, every effort should be made to verify that the needle is actually in the joint. Periarticular deposition of local anesthetic solution in this location can induce temporary radial nerve dysfunction, and horses may lose the ability to extend the carpus and digit.43 Twenty to 25 mL of local anesthetic solution are used. An older approach relied on injection of local anesthetic solution into the ulnaris lateralis bursa, once universally thought to communicate with the elbow joint. The frequency of communication between the elbow joint and ulnaris lateralis bursa was determined to be 37.5%, and therefore this approach is no longer recommended.44 We prefer to perform arthrocentesis in the proximolateral aspect of the caudal pouch in the palpable depression cranial to the olecranon process and caudal to the lateral epicondyle of the humerus. In most horses the site of needle penetration is 3 to 3.5 cm caudal to the lateral epicondyle (see Figure 10-19). In small horses and ponies, an 18- or 20-gauge, 4-cm needle is sufficient, but in large horses a 9-cm spinal needle is often necessary because the injection site is at the distal extent of the lateral head of the triceps muscle. The needle is advanced for 5 to 7 cm in a distal, slightly cranial, and medial direction until synovial fluid is recovered. However, this technique is often less well tolerated by difficult horses compared with the cranial pouch technique. Elimination of skin sensitivity at the site of needle insertion by depositing a small volume of local anesthetic solution may facilitate elbow arthrocentesis, because numerous attempts may be necessary. Synovial fluid is consistently retrievable from the joint with proper needle positioning.

Scapulohumeral (Shoulder) Joint

The shoulder joint is frequently blamed for lameness in many horses but, based on the results of diagnostic analgesia, is an uncommon source of pain. Arthrocentesis of this joint is most commonly performed at a site between the cranial and caudal prominences of the greater tubercle of the humerus, just cranial to the infraspinatus tendon. This tendon is easily palpated in most horses and serves as the primary landmark. Firm, careful palpation between the cranial and caudal prominences reveals a depression or notch, which is the point of needle insertion (see Figure 10-19). Identification of landmarks is easier in horses with muscle atrophy resulting from chronic lameness. In most horses an 18- to 20-gauge, 9-cm spinal needle is preferred, although using the entire length is not necessary. Elimination of skin sensitivity is usually not necessary. The needle is inserted in a caudomedial direction (about 45 degrees from lateral), and directed slightly distally. Attaching a syringe to aspirate synovial fluid is sometimes necessary, because in joints with minimal effusion, confirming intraarticular position of the needle may be difficult. A total of 25 to 30 mL of local anesthetic solution is used, and the horse is assessed 10 and 30 minutes after injection, because severe pain associated with osteochondrosis may resolve slowly. Analgesia of the suprascapular nerve and subsequent supraspinatus and infraspinatus muscle paralysis were reported after attempts at intraarticular shoulder

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Infraspinatus muscle

d Deltoid tuberosity Triceps brachii muscle

b c d

Biceps brachii muscle

a

Scapula

e

Olecranon

Fig. 10-19  •  Lateral view of the left elbow and shoulder regions. For arthrocentesis of the cranial pouch of the elbow (cubital) joint, the clinician directs the needle (a) medially and slightly caudally to a depth of about 5 to 6 cm at a point about 3.5 cm proximal to the lateral tuberosity of the radius and 2.5 cm cranial to the lateral collateral ligament. Arthrocentesis of the proximal, caudal pouch (b) is performed at a site in the palpable depression between the cranial aspect of the olecranon and the caudal aspect of the lateral epicondyle of the humerus. One injection site is for the rarely performed technique of synoviocentesis of the olecranon bursa (c). Proximally is the site for arthrocentesis of the scapulohumeral joint (d). A needle is inserted cranial to the infraspinatus tendon in the notch between the cranial and caudal eminences of the greater tubercle of the humerus and advanced in a caudomedial direction, roughly parallel to the ground and about 45 degrees to the long axis of the body (inset). For the bicipital bursa (e), the clinician inserts the needle at a point about 4 cm proximal to the palpable distal aspect of the deltoid tuberosity of the humerus (or alternatively, a point about 3 to 4 cm distal and 6 to 7 cm caudal to the palpable aspect of the cranial process of the greater tubercle) and directs it proximally and medially, and in some patients slightly cranially.

analgesia.43 This complication is uncommon, in our experience, and may result from proximal periarticular injection of local anesthetic solution. An alternative explanation is anesthetic solution diffusion to nerves of the brachial plexus.5 Trauma from numerous needle insertions or injection of large volumes of local anesthetic solution (>30 mL) may increase the likelihood of this complication. In fact, some have recommended using only 8 to 10 mL, but falsenegative results from the block would likely occur.43 Our opinion is that the most likely cause of this rare complication is malposition of the needle or iatrogenic trauma. Rarely, a communication between the bicipital bursa and the shoulder joint occurs.45 Thinking a horse has shoulder joint pain is possible then, but in reality the diagnosis is bicipital bursitis or tendonitis. Rather than a communication between the structures, the most likely explanation is inadvertent penetration of the bicipital bursa from a misdirected needle.

ANALGESIA OF FORELIMB BURSAE AND TENDON SHEATHS In most instances, analgesia of bursae and tendon sheaths is achieved using perineural techniques, but in some horses, selective intrasynovial analgesia is indicated. Pain sensation from bursae and sheaths is likely complex, and lameness after intrabursal or intrathecal (within a sheath) analgesia may improve but not completely resolve. In fact, horses with severe lameness resulting from bursitis or tenosynovitis often have other associated soft tissue damage, a fact that explains partial improvement after intrasynovial analgesia. Extra time is usually given, after blocking, to reassess the horse’s clinical signs.

Podotrochlear (Navicular) Bursa

As was noted previously (see DIP joint analgesia), analgesia of the navicular bursa has generally been regarded as the

Chapter 10  Diagnostic Analgesia

most specific block for diagnosis of navicular syndrome. Although likely still true, the results of at least two studies suggest there is potential for misinterpretation of the results of analgesia of the navicular bursa, and we question the specificity of the block. With a setscrew model used to induce solar pain, it was shown that injection of 3.5 mL of local anesthetic solution into the navicular bursa significantly reduced lameness scores in horses with pain at the dorsal aspect of the sole (but not the palmar aspect) within 15 minutes.29 In a complementary study using endotoxininduced synovitis of the DIP joint, injection of the navicular bursa with 3.5 mL of local anesthetic solution had no effect on lameness score at 10 minutes, but lameness was substantially decreased 20 minutes after injection (though not to a statistically significant degree [P = .07]).30 Nonetheless, the clinical experience of one of the Editors (SJD) indicates that intrathecal analgesia of the navicular bursa is reasonably reliable in improving pain associated with lesions of the navicular bone, navicular bursa, and distal aspect of the DDFT, whereas pain associated with the collateral ligaments of the DIP joint is not affected. A palmar midline approach is most commonly used for analgesia of the navicular bursa. Because needle position is difficult to assess and fluid recovery varies, radiographs should be used to confirm proper needle position. Alternatively radiodense contrast medium can be injected together with the local anesthetic solution, and a lateromedial radiographic image can then be obtained to determine that the injection was into the navicular bursa. Positioning the foot on a wooden block can minimize the problems of manipulation at the bulbs of the heel and helps to maintain aseptic technique. Subcutaneous deposition of a small volume (1 to 2 mL) of local anesthetic solution can improve horse compliance during this procedure. An 18- to 20-gauge, 9-cm

spinal needle is inserted on the palmar midline, just proximal to the hairline, and directed parallel to the sole until the needle contacts bone (Figure 10-20).25,27,46 Others describe a similar approach, although they direct the needle parallel to the coronary band.21,47,48 Because redirection of the needle proximally or distally often is necessary, these approaches differ little. Success depends most on personal experience, but radiographs can be critical in confirming successful entry into the navicular bursa. The direction in which the needle is inserted is often dictated by the shape of the horse’s foot and the projected position of the navicular bone.5 Plotting and marking the navicular position on the hoof wall can be helpful in determining needle direction and depth of insertion. The navicular position is located at a site 1 cm distal to and halfway between the dorsal and palmar aspects of the coronary band.48,49 However, with experience and after identifying the navicular position, the procedure can be done blindly. In most horses the flexor surface of the navicular bone will be contacted at a depth of 4 to 5 cm. The needle is likely improperly positioned if resistance is encountered at a depth of less than 3 to 4 cm or if the needle can be advanced more than 6 to 7 cm. Spontaneous retrieval of synovial fluid is rare and usually indicates that the needle is in the DIP joint capsule or the DFTS. To avoid penetrating these structures, the needle should be placed in the middle of the flexor surface of the navicular bone.5 Three to 5 mL of local anesthetic solution are used. If navicular syndrome is suspected, some clinicians combine injection of local anesthetic solution with a corticosteroid. Alternatively, navicular bursography50 can be performed in combination with diagnostic analgesia by adding 1 to 2 mL of sterile, iodinated contrast material (see Chapter 30). Because in the standing horse the navicular bursa is under compression by the DDFT, suspending the

50% 1cm

b Navicular bone

a A

123

B Fig. 10-20  •  A, Lateral view showing two techniques for synoviocentesis of the navicular bursa of the foot. In the palmar (plantar) approach (a) the needle is placed just proximal to the hairline between the bulbs of the heel and inserted to the navicular bursa using the navicular position as a guide. The navicular position (arrow) is located by determining the point on the outside of the hoof wall that is 50% of the distance from the dorsal to the palmar (plantar) extent of the coronary band and 1 cm below (inset). An approach slightly more proximal (b) requires placing the needle in the depression between the heel bulbs and advancing the needle in a dorsodistal direction, about 30 degrees from horizontal toward the navicular position. B, Palmarolateral (plantarolateral) view of the digit showing the lateral approach for synoviocentesis of the navicular bursa. The needle is inserted just proximal to the cartilage of the foot between the digital neurovascular bundle and the digital flexor tendon sheath and directed axially,  distally, and slightly dorsally.

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foot or placing the toe in a “navicular block” as if for radiography, with the foot in partial flexion during actual injection, are useful. Without using radiographs, being confident of accurate needle placement is difficult. A proximal, palmar injection technique has been described. A needle is inserted into the deepest part of the hollow between the heel bulbs and advanced dorsodistally, about 30 degrees from horizontal, until contact with the bone is made.45,51 A lateral (or medial) approach is also described. A needle is inserted just proximal to the cartilage of the foot, between the neurovascular bundle and the DFTS and directed axially, distally, and slightly dorsally until contact with bone is made (see Figure 10-20).46,48,52 These five techniques were compared in an in vitro study. The most reliable technique was determined to be the distal palmar approach, with the needle being directed to the navicular position and the limb in a non–weight-bearing position.53

Digital Flexor Tendon Sheath

Two sites for intrasynovial injection of the DFTS are just proximal to the palmar (plantar) annular ligament (PAL) or in the palmar aspect of the pastern region in an outpouching of the sheath located between the proximal and distal digital annular ligaments (see Figure 10-17). Effusion facilitates identification of these sites, and rarely would an intrathecal injection be contemplated without the presence of effusion. Proximal to the PAL, villous hypertrophy of synovial membrane can complicate the procedure, because even with severe distention of the sheath, synovial fluid may be difficult to retrieve. For this reason we favor the palmar pastern approach. In some horses the sheath appears to be compartmentalized and distended proximal to the PAL but not below, and therefore injections are easier to perform proximally. A 20-gauge, 2.5-cm needle and 10 to 15 mL of local anesthetic solution are used (see also Figure 124-1). In contrast to intrasynovial analgesia in other locations in the digit, analgesia of the DFTS appears to be quite specific for lameness associated with pain arising from structures contained within it.54 In other words, unless local anesthetic solution is inadvertently injected outside of the DFTS or leaks from it after injection, analgesia of nearby digital nerves and structures appears unusual. However, local diffusion may result in alleviation of pain from the oblique or straight sesamoidean ligaments.55 Alternatives to these approaches for intrasynovial injection of the DFTS are described. The procedure can be performed at a site just distal to the PSBs, between the distal aspect of the PAL and the proximal aspect of the proximal digital annular ligament (see Figure 10-17). A palmar axial sesamoidean approach has been described. With the metacarpophalangeal joint held in flexion (225-degree angle between the McIII and the proximal phalanx), a 20-gauge, 2.5-cm needle is inserted at an angle of 45 degrees, 3 mm axial to the palmar border of the PSB (midbody) and just palmar to the neurovascular bundle. Putative advantages included more reliable access to the DFTS when effusion is absent and reduced time required for successful entry.56

Carpal Sheath

The carpal sheath (carpal flexor sheath) envelops the SDFT and DDFT in the carpal canal. Distention of the carpal sheath is most easily recognized laterally, just proximal to

the accessory carpal bone, between the lateral digital extensor and ulnaris lateralis tendons (see Figure 10-18). Effusion of the carpal sheath must be differentiated from that of the antebrachiocarpal joint. Concurrent distention of the dorsal aspect of the antebrachiocarpal joint or distention of the distal aspect of the carpal sheath (lateral or medial, distal to the flexor retinaculum on the palmar aspect of the metacarpal region) is a sign that is helpful in determining this. Ultrasonographic evaluation or positive contrast radiography can be useful adjunct diagnostic techniques. Synoviocentesis can be performed in either the proximal or the distal aspect of the sheath, using a 20-gauge, 2.5-cm needle and 10 to 15 mL of local anesthetic solution.

Olecranon Bursa

This technique is mentioned to be complete, but we have never found an indication to perform analgesia of this bursa (see Figure 10-19). If distended, this bursa could be entered using the same techniques described for other bursae. Rarely, local analgesia over implants used to repair olecranon process fractures is necessary to investigate whether implant removal is indicated.

Bicipital Bursa

Bicipital bursitis and shoulder lameness are frequently diagnosed but in reality are uncommon causes of lameness, if the clinician religiously adheres to the principles of diagnostic analgesia. However, bicipital bursitis and tendonitis and proximal humeral osteitis, fractures, or osseous cystlike lesions can cause lameness and are diagnosed using analgesia of the bicipital bursa. The bicipital bursa is located between the greater and lesser tubercles of the humerus and the overlying tendon of origin of the biceps brachii muscle. Synoviocentesis of the bicipital bursa is routinely performed from a lateral approach, but if severe effusion exists, the bursa can be accessed medially. The injection site is located just cranial to the humerus, 4 cm proximal to the distal aspect of the deltoid tuberosity.46 Alternatively, the site can be located by finding a point 3 to 4 cm distal and 6 to 7 cm caudal to the cranial process of the greater tubercle (see Figure 10-19).19 Subcutaneous infiltration of local anesthetic solution at the site can be used but is rarely needed. An 18-gauge, 9-cm needle is directed in a proximal, medial, and slightly cranial direction and can be “walked off” (shaft of the needle in contact with the bone) the cranial cortex of the humerus. A change in resistance is felt, and synovial fluid may be seen in the needle hub or can be aspirated. Ten to 20 mL of local anesthetic solution are used. If injection is difficult, synovial fluid cannot be retrieved, and retrieving local anesthetic solution already injected is not possible, the bursa likely has not been entered. A recent study showed a high failure rate of injection with either technique.57 Moreover, false-negative results also occur, despite retrieval of synovial fluid, in association with severe lesions of the tendon of biceps brachii or in the presence of dystrophic mineralization or ossification.58 An alternative is to use an ultrasound-guided technique, which may be more accurate.

PERINEURAL ANALGESIA IN THE HINDLIMB Perineural analgesia in the distal aspect of the hindlimb is similar to that described for the forelimb. Minor differences

in innervation and anatomy must be taken into consideration, however. Technical differences in whether, or how, the limb is held and other intangible differences exist. Most clinicians are not as familiar, or frankly as comfortable, with performing hindlimb analgesic techniques, and this is particularly true with perineural analgesia. It takes a dedicated lameness detective to be enthusiastic about hindlimb analgesia, particularly in fractious or highly strung horses. Obviously, safety for the veterinarian and assistants is paramount, and physical and chemical restraint become important. Performing intraarticular analgesia is far easier, but the clinician must keep in mind that perineural techniques are much more effective in abolishing subchondral bone pain. Therefore false-negative results will likely be obtained if one is limited to only intraarticular procedures. We generally recommend that most perineural techniques distal to the tarsus be performed with the limb held off the ground by an experienced assistant, but personal preference can of course prevail. In some instances, such as when plantar digital analgesia is performed, the anatomy is much easier to identify when the limb is bearing weight. One of the Editors (SJD) routinely performs the majority of hindlimb local analgesic techniques with the limb bearing weight, and with the horse restrained in wooden stocks. The hindlimb can be positioned behind or just in front of the back wooden post; the clinician is then protected by the post if the horse kicks. To limit the number of hindlimb injections in horses that lack clinical signs referable to the digit, starting with the low plantar block (low 4 point or 6 point block) may be reasonable, in lieu of performing sequential blocks starting with plantar digital analgesia. Of course, performing blocks distal to this site at another time may be necessary if baseline lameness is discovered using this approach. The clinician should take care when testing the efficacy of hindlimb blocks, and using a pole or similar device may be safer than using forceps.5 Complete abolition of skin sensation in the hindlimb is less likely than in the forelimb because the distribution of cutaneous innervation varies.

Plantar Digital Analgesia

The technique for plantar digital analgesia is essentially the same as in the forelimb (see Figure 10-5). The prevalence of lameness abolished by plantar digital analgesia in the hindlimb is considerably lower than palmar digital analgesia in the forelimb but is not zero, and therefore this block should still represent a good starting point for a horse with undiagnosed hindlimb lameness. Because of the reciprocal apparatus, the digit is constantly flexed when the limb is held off the ground, and this block can be slightly more difficult to perform in this position. However, just as in the forelimb, results can be misleading with abolition of pastern or fetlock region pain.

Dorsal Ring Block of the Pastern

The section on the dorsal ring block of the pastern in the forelimb describes this technique (see Figure 10-5). This block requires several needle insertions and can be difficult to perform if the limb is held off the ground, because the dorsal aspect of the pastern is constantly flexed, making subcutaneous injection difficult.

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125

Basisesamoid and Abaxial Sesamoid Blocks

Basisesamoid and abaxial sesamoid blocks present no essential differences between the forelimbs and hindlimbs (see Figure 10-5). Our philosophical points about the basisesamoid block (see forelimb) hold true in the hindlimb as well. The abaxial sesamoid block is avoided, if possible, in racehorses, because the high prevalence of lameness involving the metatarsophalangeal joint may lead to inadvertent misdiagnosis (a positive response to the block will be interpreted as lameness in the foot, when in reality lameness involves the metatarsophalangeal joint).

Low Plantar Block

Analgesia of the metatarsophalangeal joint region is achieved using the low plantar block, a procedure similar to the low palmar block (see Figure 10-7). This block is one of the most overlooked but most useful of all perineural techniques. It is essential to block the medial and lateral and plantar and the medial and lateral plantar metatarsal, and in some horses the dorsal metatarsal nerves. For routine diagnostic analgesia we do not block the dorsal metatarsal nerves, but for therapeutic analgesia they should be blocked. Anecdotal information suggests that some practitioners may not include the plantar metatarsal nerves when performing this block. The plantar metatarsal nerves supply innervation to the subchondral bone of the distal aspect of the third metatarsal bone (MtIII), and to provide analgesia to this important area, these nerves need to be blocked. In fact, a modification of this technique can be used in horses suspected of having subchondral, maladaptive, or nonadaptive remodeling of the MtIII, a common diagnosis in Standardbred and Thoroughbred racehorses (see Chapters 106 to 109). A positive response to an independent block of the lateral plantar metatarsal nerve can help establish this syndrome as the cause of lameness. Other causes of pain arising from the lateral aspect of the metatarsophalangeal joint, including fractures of the lateral condyle of the MtIII or of the PSBs, can be abolished using this modified technique. The only difference between the low palmar and low plantar blocks involves the dorsal aspect of the limb (see Figure 10-7). Skin sensation laterally and medially is retained after this block, unless a circumferential, subcutaneous ring block is used. In the forelimb, it is necessary to use subcutaneous infiltration only to the dorsal midline. Alternatively, the dorsal metatarsal nerves can be blocked individually.

High Plantar Nerve Block

The high plantar or subtarsal block is one of the most important but often overlooked perineural analgesic procedures in the horse. This block is used to diagnose suspensory desmitis, arguably one of the most important lameness conditions in the hindlimb. However, suspensory desmitis can be a catchall diagnosis in some horses with occult hindlimb lameness, and the high plantar block must be done to confirm the authentic location of pain. The high plantar block should be done after completion of lower limb blocks such as low plantar analgesia to rule out other common sources of pain. Practitioners should be wary of a recent trend to complete only a subtarsal block to diagnose, erroneously in some horses, proximal suspensory desmitis, when sequential distal-to-proximal analgesic

126

PART I  Diagnosis of Lameness Tibial nerve Medial plantar nerve

Lateral plantar metatarsal nerve Lateral plantar nerve

Medial plantar metatarsal nerve Medial plantar nerve

Lateral plantar nerve Deep branch of lateral plantar nerve

Lateral and medial plantar metatarsal nerves

Fig. 10-22  •  The high plantar block is performed at a level 4 cm distal to the proximal aspect of fourth metatarsal bone and on the medial side 3 cm distal to the proximal aspect of second metatarsal bone. The needles are inserted axial to the respective splint bone and advanced deep to contact the plantar surface of the third metatarsal bone. Local anesthetic solution is deposited in this location to block the lateral (medial) plantar metatarsal nerves and in a more superficial position as the needle is withdrawn blocks the lateral (medial) plantar nerves (inset).

Fig. 10-21  •  Positive contrast arthrogram of the tarsometatarsal joint showing short, distoplantar outpouchings extending distally toward the origin of the suspensory ligament. Inadvertent penetration of these pouches occurs during subtarsal or high plantar analgesic techniques.

techniques may have revealed an alternative source of pain. The tarsometatarsal joint has distoplantar outpouchings (similar to but less extensive than the distopalmar outpouchings of the carpometacarpal joint) that may complicate tarsometatarsal intraarticular or high plantar analgesic techniques (Figure 10-21). However, this is certainly less of a problem in the hindlimb than in the forelimb. For example, inadvertent penetration of the tarsometatarsal joint occurred in only 5% of limbs in which high plantar analgesia was performed, at a level of 1.5 cm distal to the tarsometatarsal joint. However, contrast material was found in the tarsal sheath in 40% of limbs, adding yet another dimension to this already somewhat difficult blocking technique. False-negative results have been attributed to inadvertent injection into blood or lymphatic vessels.59 The clinician should take care in preparing the limb for this procedure and interpreting the results. It is possible, although not likely, that when a high plantar block is performed, local anesthetic solution could be inadvertently placed in the tarsometatarsal joint. A good chance also exists, however, of inducing analgesia of the tarsal sheath. Comprehensive evaluation using numerous imaging modalities is needed when attempting to differentiate causes of lameness in this important area. The medial and lateral plantar and the medial and lateral plantar metatarsal nerves are blocked, and a circumferential dorsal ring block provides complete analgesia to the metatarsal region. Blocking only the plantar metatarsal nerves can abolish pain associated with the suspensory

ligament. Most clinicians do not include the dorsal ring block, but it is necessary to do so to eliminate lameness resulting from injury of the dorsal cortex of the MtIII or to suture lacerations in this area. This block is performed most commonly and safely with the limb held off the ground. Although uncommon to rare, needle breakage is a complication during high plantar analgesia, and for this reason we prefer to use needles no smaller than 18 to 20 gauge and 4 cm long. At this level on the plantar aspect of the limb, it is impossible to palpate nerves, and unlike with the high palmar block, only one injection site exists for each, on the medial and lateral aspects of the limb. The needle is placed just distal to the tarsometatarsal joint and axial to the fourth metatarsal bone (MtIV) and inserted until contact is made with the MtIII (Figure 10-22). A minimum of 5 mL of local anesthetic solution is deposited at this deep location, and an additional 5 mL are deposited as the needle is withdrawn, leaving a definite bleb in the subcutaneous tissues. Some clinicians prefer lower volumes of local anesthetic solution. Additional local anesthetic solution can be used without risk, and a common modification is flooding the origin of the suspensory ligament with an additional 5 to 10 mL of local anesthetic solution. The procedure is then repeated medially, and the needle is inserted axial to the second metatarsal bone (MtII). To complete the block, a circumferential subcutaneous ring block is performed. The clinician must take care not to lacerate the dorsal metatarsal artery or the saphenous vein during this procedure. An alternative technique to alleviate pain from the proximal aspect of the suspensory ligament is to block the deep branch of the lateral plantar nerve. This can be performed with the limb bearing weight or lifted, according to personal preference. A 20-gauge needle is inserted perpendicular to the skin just plantar to the MtIV at the

Chapter 10  Diagnostic Analgesia

junction where its contour changes from oblique to vertical. The needle is inserted to a depth of approximately 1 cm, and 3 mL of local anesthetic solution are deposited. This block is quick and easy to perform and is generally well tolerated but may not remove pain associated with entheseous reaction.5 See the following text for a discussion of alternative techniques to block the suspensory origin.

Fibular (Peroneal) and Tibial Nerve Blocks

Analgesia of the distal crus and tarsus or entire distal aspect of the hindlimb is induced using the fibular and tibial nerve blocks. These blocks are used most commonly in horses with distal hock joint pain, in which intraarticular analgesia is difficult or impossible to perform. The fibular and tibial nerve blocks, when completed successfully, are more effective in eliminating pain from the complex hock joints than is intraarticular analgesia. The fibular and tibial nerve blocks also are useful in eliminating pain associated with subchondral trauma of the distal aspect of the tibia and talus, distally located tibial stress fractures, the tarsal sheath, the distal aspect of the common calcaneal tendon, the calcaneal bursa, and the plantar aspect of the hock. The clinician should keep in mind that if the high plantar block has not already been performed, the fibular and tibial nerve blocks eliminate pain associated with proximal suspensory desmitis. The deep fibular nerve is blocked at a site located laterally, 10 cm proximal to the point of the hock (tuber calcanei), in the groove between the long and lateral digital extensor muscles (Figure 10-23). In this groove the superficial fibular nerve is easily palpated and can be rolled against the fascia of the crus. An 18- to 22-gauge, 4-cm needle is inserted to the hub or until it contacts the lateral tibial cortex, and 10 to 15 mL of local anesthetic solution

Deep fibular (peroneal) nerve

b Tibial nerve

a Superficial fibular (peroneal) nerve

Lateral digital extensor

Fig. 10-23  •  Lateral view of the left crus and tarsus showing the fibular (peroneal) and tibial nerve block. The deep and superficial fibular nerves are blocked by finding the groove between the long and lateral digital extensor muscles, 10 cm proximal to the tarsus, in which the superficial fibular nerve is palpable. The needle (a) is advanced deep to block the deep branch and withdrawn to a more superficial position to deposit local anesthetic solution subcutaneously to block the superficial branch. The tibial nerve block (b) is performed by palpating the nerve just cranial to the common calcaneal tendon (from either a lateral or a medial approach) in a location about 10 cm proximal to the tuber calcanei.

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are injected, beginning deep and continuing as the needle is withdrawn. The needle can be redirected in a fan-shaped pattern if desired to ensure complete block of the deep branch of the fibular nerve. Seeing blood in the needle hub is common, a reliable sign of accurate needle placement, because the cranial tibial vein and artery are located close to the deep fibular nerve.60 Performing the tibial block first is therefore preferable, as is warning the client that blood may appear.5 The superficial fibular nerve is blocked as the needle is withdrawn from deep within the injection site. Additional local anesthetic solution (5 to 10 mL) is placed in this subcutaneous location. The tibial nerve is blocked at a site 10 cm proximal to the tuber calcanei, cranial to the common calcaneal tendon, and caudal to the DDFT (see Figure 10-23). The nerve can be palpated as a firm cordlike structure with the limb in a flexed position. For this reason, performing this block may be easier with the limb not bearing weight. Although the tibial nerve is slightly more superficial medially, the injection can be performed either medially or laterally. A 20-gauge, 2.5-cm needle is inserted laterally, and 15 mL of local anesthetic solution are injected over the nerve. The needle tip should be palpated under the skin, medially, to ensure the proper depth of penetration. Local anesthetic solution can be placed using a fan-shaped injection technique, but the horse will object if the tibial nerve is penetrated. Although deep pain will be abolished if these nerves are successfully blocked, superficial sensation persists on the medial aspect and occasionally in the caudal (plantar) aspect of the limb. To use the fibular and tibial nerve blocks therapeutically, it is necessary to perform a circumferential subcutaneous ring block to completely abolish skin sensation. After the fibular and tibial nerve blocks, paradoxically, preexisting toe drag may persist or increase, despite resolution of weight-bearing lameness.5 Some horses stumble or knuckle, indicating loss of extensor muscle function, but this is not common and certainly not a necessary sign to suggest that complete analgesia has been obtained. However, exercising a horse at speed or over fences should be avoided. Because of nerve size and depth, we suggest that additional time be given, as much as 20 to 30 minutes, to evaluate the effect of this block before a final conclusion is reached. Dyson has recognized improvement in horses up to 1 hour after blocking and warns that proceeding with a stifle block too soon leads to false-positive results.5 The fibular and tibial nerve blocks are not commonly performed in practice, at least in the United States, and at best may result in only 50% to 80% improvement in lameness score, particularly in those horses with severe distal hock joint pain, although in some horses lameness is abolished completely. Allowing more time for maximal response and taking a realistic approach to the percent improvement expected are warranted when using the fibular and tibial nerve blocks. Intrasynovial analgesic techniques are certainly more specific than are the fibular and tibial nerve blocks, and although the fibular and tibial nerve blocks have limitations, the lameness diagnostician should become familiar and comfortable with this procedure. Proficiency in performing these blocks is a must for accurate diagnosis of hindlimb lameness. Performing the fibular and tibial components can independently improve specificity of the fibular and tibial nerve blocks.

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INTRAARTICULAR ANALGESIA IN THE HINDLIMB Analgesia of the DIP and proximal interphalangeal joints in the hindlimb is exactly the same as that described for the forelimb. Performing intraarticular analgesia of the metatarsophalangeal joint is the same as that described for the metacarpophalangeal joint. Perineural analgesic techniques should be used whenever possible, because subchondral bone pain is more completely abolished with these techniques, and false-negative results are less likely.

Tarsus Tarsometatarsal Joint

The most reliable site for arthrocentesis of the tarsometatarsal joint is a lateral approach, just proximal to the MtIV. At this site is a subtle but consistent depression that can reliably be palpated. A 20-gauge, 2.5-cm needle is inserted in a dorsomedial and slightly distal direction (Figure 10-24). The needle can usually be inserted to the hub, but occasionally it hits articular cartilage. Synovial fluid is consistently retrieved, but we find it interesting that even in horses without lameness of the tarsometatarsal joint, the fluid is generally watery, lacking what is thought to be normal viscosity. In most horses, up to 4 mL of local anesthetic solution can usually be injected without encountering elevated intraarticular pressures and horse discomfort. Be aware that beyond 2 mL the horse may start to feel uncomfortable, raise the limb, or even kick. Anecdotal reports of a subtle pop or sudden decrease in pressure have

been attributed to communication between the tarsometatarsal and centrodistal (distal intertarsal) joints. In reality, this most often results from rupture of the tarsometatarsal joint capsule and subsequent deposition of local anesthetic solution (or medication) extraarticularly into the tarsal space and not the centrodistal joint. We recommend using no more than 4 mL of local anesthetic solution or injecting only that amount of local anesthetic solution necessary to develop moderate intraarticular resistance to avoid inadvertent deposition into the intertarsal space. Periarticular extravasation of local anesthetic solution from excessive volume may inadvertently block the nearby lateral plantar nerve and deep branch, potentially alleviating pain associated with the suspensory ligament attachment or other structures. An alternative site for tarsometatarsal arthrocentesis is a medial approach, similar to that described for the centrodistal joint. The issue of communication between the distal tarsal joints is important from diagnostic and therapeutic standpoints. Studies have shown that the tarsometatarsal and centrodistal joints communicate in 8% to 35% of normal horses.59,61,62 Communication between the tarsometatarsal joint (and presumably the centrodistal joint) and the talocalcaneal-centroquartal (proximal intertarsal) and tarsocrural joints was shown to be about 4% in an in vivo study, after injection of latex in the tarsometatarsal joint.62 Some concern and confusion exist regarding whether or not a single injection into the tarsometatarsal joint also provides analgesia or treats the centrodistal joint. Some clinicians even preferentially inject a large volume of local anesthetic solutions or drugs, hoping to block or medicate the

Joint capsule

c

c a b

Tendon sheath

a

Joint capsule

a

Mt IV Joint capsule Saphenous vein

A

Cunean tendon

Cunean bursa

B

b

Fig. 10-24  •  A, Lateral and plantar (inset) views of the left tarsus showing sites for tarsal arthrocentesis. The tarsometatarsal joint is entered by locating the depression just proximal to the proximal aspect of the fourth metatarsal bone (Mt IV) and inserting a needle (a) in the plantar aspect of this depression, directing it dorsomedially. The dorsomedial pouch of the tarsocrural joint (b) is entered either just lateral or medial to the dorsal branch of the saphenous vein or, alternatively, using the plantarolateral pouch (c). B, Medial view of the left tarsus. The centrodistal joint is entered by placing the needle (a) in the depression formed between the fused first and second tarsal bones, the third tarsal bone, and the central tarsal bone, which is at the proximal edge or just slightly distal to the proximal edge of the cunean tendon. The cunean bursa (dashed ellipse) is entered by locating the distal border of the cunean tendon and inserting the needle (b) under the tendon from the distal aspect or placing it directly through the tendon. The distended tarsal sheath (c) can be entered proximal, just caudal to the tarsocrural joint capsule or distal (not shown) to the tarsus.

tarsometatarsal and centrodistal joints. A recent in vitro study found that, although gross anatomic communications exist in only a minority of horses, diffusion of mepivacaine between the distal tarsal joints (as well as between the distal tarsal joints and the tarsocrural joint) occurs with a much higher frequency. Fifteen minutes after injection of 5 mL of 2% mepivacaine into either the tarsometatarsal or the centrodistal joint, mepivacaine was detected in the alternate joint at concentrations >300 mg/L in 64% and 60% of specimens, respectively.63 Whether or not this holds true in the live horse remains undetermined. For that reason, and based on our clinical experience, we believe the clinician should still consider the tarsometatarsal and centrodistal joints to be separate synovial cavities. However, it is clear that in some horses analgesia or treatment of the tarsometatarsal joint will relieve centrodistal joint pain. Because the tarsometatarsal joint has distoplantar outpouchings, abolishing pain associated with the proximal suspensory attachment or lesions involving the proximal aspect of the MtIII is also possible when performing tarsometatarsal analgesia. Accurate differential diagnosis for pain involving the lower hock joints and proximal metatarsal region depends on careful interpretation of response to diagnostic analgesia and evaluation of ancillary images.

Centrodistal Joint

Compared with the tarsometatarsal joint, arthrocentesis of the centrodistal joint is relatively difficult. The centrodistal joint is small, and in fact inserting a needle any larger than 22 to 25 gauge into this joint is difficult, even in horses with normal width of joint space. We have tried several alternative sites, including dorsomedial and dorsolateral approaches. Anecdotal reports suggest that the dorsomedial approach, about 1 cm distal to the distal end of the medial trochlear ridge, is a consistent, reliable injection site, but we often enter the proximal intertarsal joint from this approach. An outpouching of the centrodistal joint exists dorsolaterally, but we reasoned that the perforating tarsal artery precluded use of this site in vivo. A recent study described the use of this dorsolateral approach. The site is identified as a point 2 to 3 mm lateral to the long digital extensor tendon and 6 to 8 mm proximal to a line drawn perpendicular to the long axis of the MtIII at the level of the proximal aspect of the MtIV. The success rate for arthrocentesis at this site was equal to that for the traditional medial approach, with purported advantages being improved safety for the clinician and easily identified landmarks. In vivo, iatrogenic injury to the dorsal pedal artery or penetrating tarsal artery was not encountered.64 We still preferentially use a medial approach at the distal aspect of, or through, the cunean tendon (medial tendon of insertion of the tibialis cranialis muscle), a structure that can be readily palpated. With a fingertip, the distal edge of the cunean tendon is moved proximally to reveal an ill-defined concavity, the articulation of the fused first and second tarsal bones, with the third and central tarsal bones (see Figure 10-24). This depression is sometimes located in a slightly more proximal location. This injection technique is one of the few commonly performed by standing on the opposite side of the horse. A skin bleb is useful because in most horses inserting a needle directly into the joint is difficult, and numerous attempts may be necessary. A 22- to 25-gauge, 2.5-cm needle is inserted

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directly in a lateral direction, horizontally, roughly parallel to the central and third tarsal articulation, perpendicular to the skin. Slight redirection of the needle may be necessary, and in many horses joint fluid is not obtained. If the needle can be inserted to a depth of 1 to 1.5 cm, it is likely properly positioned even if synovial fluid cannot be retrieved. Fluid retrieved in a more superficial location likely indicates penetration of the cunean bursa. In horses in which diagnostic information or therapeutic injection is critical and any question of needle placement exists, radiographs are warranted. A maximum of 4 to 5 mL can be injected. If a larger volume can be comfortably injected, the needle tip is likely in the tarsal space or in the proximal intertarsal joint, or a communication with the tarsometatarsal joint exists. If the injection is difficult to perform, the needle is likely malpositioned in the subcutaneous tissues, or the needle tip is touching articular cartilage. Most clinicians attempt injection of the centrodistal joint after first injecting the tarsometatarsal joint, and in some instances, medication or local anesthetic solution readily flows from the needle. The typical response is, “There must be a communication between the tarsometatarsal and centrodistal joints.” However, this clinical finding most often results from inadvertent penetration of the distended medial pouch of the tarsometatarsal joint. Fluid accumulation in the tarsal space from the tarsometatarsal joint injection can cause the same result, if the needle enters the tarsal space rather than the centrodistal joint space. In horses with advanced osteoarthritis or even in horses with early distal hock joint pain, it may be difficult or impossible to be confident that intraarticular analgesia has been achieved. An alternative approach for providing tarsal analgesia is first to perform sequential, intraarticular analgesia of the tarsometatarsal and tarsocrural joints, and then to perform the fibular and tibial nerve blocks if lameness persists. If lameness abates after the fibular and tibial nerve blocks, a presumptive diagnosis of centrodistal joint pain can be made, assuming other sources of pain abolished by this block can be ruled out.

Tarsocrural Joint

Arthrocentesis of the tarsocrural joint is straightforward and easy compared with some joints, because of extensive and multiple dorsal and plantar outpouchings. In horses with moderate to severe effusion, identifying four distinct outpouchings—the dorsolateral, dorsomedial, plantarolateral, and plantaromedial pouches—is easy. The clinician must keep in mind that the tarsocrural and proximal intertarsal joints communicate through a large fenestration at the dorsal aspect of the joints in adult horses, although in weanlings and yearlings the fenestration often cannot be seen during arthroscopic examination. Any one of the tarsocrural joint pouches can be used, but the most common site of entry is on either side of the saphenous vein, in the dorsomedial pouch (see Figure 10-24). This particular site is preferred in horses without obvious effusion. An alternative site is the plantarolateral pouch. The most consistent site to use is the distal aspect of the dorsomedial pouch, just distal to the medial malleolus of the tibia and medial to the saphenous vein. An 18- to 20-gauge, 2.5- or 4-cm needle is used to deposit 20 to 30 mL of local anesthetic solution into the tarsocrural joint. In horses with severe osteoarthritis of the tarsocrural joint or those with

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subchondral bone pain, use of as much as 30 to 50 mL of local anesthetic solution is necessary to abolish pain. In these horses, a false-negative result is common if only 10 to 20 mL of local anesthetic solution is used. The plantar pouches can be useful alternative sites for arthrocentesis if the dorsomedial pouch is unsuitable, as sometimes occurs with a wound, swelling associated with trauma of the fibularis (peroneus) tertius, or superficial dermatitis. The plantar pouches must be differentiated from distention of the tarsal sheath or other forms of thoroughpin. Although the dorsal and plantar pouches freely communicate, anatomically, flushing from one aspect of the tarsocrural to the other when the horse is in a weightbearing position may be difficult. Fluid flow between articular surfaces and joint spaces under collateral ligaments is likely restricted when horses are in a weight-bearing position. This same phenomenon occurs in other joint spaces.

Stifle Joint

The three compartments of the equine stifle joint are the medial femorotibial, lateral femorotibial, and femoropatellar joint compartments. Most consider that the femoropatellar and medial femorotibial joints communicate in almost all horses and that the lateral femorotibial compartment is solitary, but recent anatomical studies have shed new light on this time-honored concept. The frequency of communication between the medial femorotibial and femoropatellar compartments was found to be 60% to 74% in normal horses when the injection was performed from the femoropatellar compartment.65,66 The frequency of communication was higher (80%) when the injection was performed in the medial femorotibial compartment.65 It is important to realize, however, that the medial femorotibial and femoropatellar compartments did not communicate in all horses. Inconsistency in communication depending on which compartment was injected was attributed to directionality in the normal foramen or slit between the two compartments (flow easier from the medial femorotibial to the femoropatellar compartment). The time-honored assumption that the lateral femorotibial joint is a solitary compartment was also challenged. The lateral femorotibial joint communicated with the femoropatellar joint in 3% to 18% of horses but was indeed solitary in the majority of normal horses.65,66 Communication may be more frequent after trauma and certainly after arthroscopic surgical procedures. Similar to the digit, carpus, and tarsus, there is clinically important evidence that mepivacaine diffuses between the compartments of the stifle joint. The proportion of synovial compartments with mepivacaine concentration >300 mg/L 15 minutes after injection of an adjacent compartment with 10 mL of 2% mepivacaine ranged from 5% to 40%.63 Of note, functional (diffusion) communication between the medial femorotibial and femoropatellar joints was lower than previous estimates (25% to 40% versus 60% to 80%). Volume of local anesthetic solution (10 mL) was considerably lower than is commonly used in clinical practice for intraarticular analgesia of the stifle joints, and it remains undetermined if results of in vitro studies translate to actual clinical relevance. We recommend that each compartment of the stifle joint be injected independently, either sequentially or simultaneously, to avoid confusing results during stifle

analgesia. The variable degree of communication will obviously cause some degree of uncertainty in diagnosis. The same principle is recommended for therapy as well. Needle insertion in the stifle joints is complicated by a natural tendency of horses to react inappropriately to manipulation compared with other areas of the limbs. Horses seem to object to simple palpation of the stifle and may become fractious during arthrocentesis. To avoid excessive manipulation during injection, we have found it useful to attach an extension set to the needle, a procedure that obviates the need to touch the needle or skin when attaching the syringe. If necessary, the extension set may be useful for many diagnostic procedures, particularly in the hindlimbs. In general, 20 to 30 mL of local anesthetic solution are used in each of the medial femorotibial, lateral femorotibial, and femoropatellar compartments. A common misconception is that long needles are needed to perform arthrocentesis of the stifle joint compartments. In fact, some racehorse trainers will insist that “the long needles, Doc” are necessary to achieve success in medicating the femoropatellar joint. If arthrocentesis is performed with the limb in a weight-bearing position, the joint capsules can easily be penetrated with needles no longer than 4 cm. In the flexed position, use of a spinal needle when performing femoropatellar arthrocentesis is necessary. We prefer to have the horse in a weight-bearing position, with the limb slightly ahead of the contralateral limb, a position that allows the clinician to palpate landmarks readily without undue tension on patellar and collateral ligaments. Arthrocentesis of the medial femorotibial joint is performed at a site located just caudal to the medial patellar ligament, cranial to the medial collateral ligament, and 1 to 2 cm proximal to the medial tibial plateau (Figure 10-25). In a normal horse a distinct depression occurs at this location, but in horses with effusion, a considerable bulge in the joint capsule can be present. An 18-gauge, 4-cm needle is inserted perpendicular to the skin and can be redirected or rotated if synovial fluid is not immediately retrieved. A common mistake is to insert the needle too far distally, and in this position the needle tip enters ligaments or the medial meniscus. Arthrocentesis of the lateral femorotibial joint is more challenging than for the other two compartments, because the lateral joint pouch is small and located deep within tissue. The site is caudal to the long digital extensor tendon and cranial to the lateral collateral ligament, just proximal to the lateral tibial plateau (see Figure 10-25). These landmarks are easily palpated, but distention of the joint capsule is not, in contrast to the medial femorotibial joint. An 18-gauge, 4-cm needle is inserted horizontally and directed in a slight caudomedial direction. Retrieval of synovial fluid varies, and redirecting or rotating the needle is often necessary. An alternate site can be used, located caudal to the lateral patellar ligament and cranial to the long digital extensor tendon, and just proximal to the tibial plateau. Arthrocentesis of the femoropatellar joint is most commonly performed at a sub-patellar site and either lateral or medial to the middle patellar ligament. The joint capsule can be easily palpated even in most normal horses, if the horse is in a weight-bearing position. With the horse in a weight-bearing position, an 18-gauge, 4-cm needle is inserted perpendicular to the skin, or directed slightly

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e

Medial patellar ligament

Lateral patellar ligament

Lateral collateral ligament

Medial collateral ligament

a

b

d

c

A

B

Long digital extensor muscle

Fig. 10-25  •  A, Cranial view of the left stifle. The medial femorotibial joint (a) is approached from a site between the medial patellar and medial collateral ligaments, about 2 cm proximal to the proximal aspect of the tibia. The femoropatellar joint (b) most commonly is injected either between the lateral and middle patellar ligaments or between the middle and medial patellar ligaments (not shown). The needle is directed proximally in this subpatellar position. B, Lateral view of the left stifle. The lateral femorotibial joint can be approached by placing the needle caudal to the long digital extensor tendon and cranial to the lateral collateral ligament (c) or inserting it between the lateral patellar ligament and the cranial edge of the long digital extensor tendon (d). An alternative site for arthrocentesis of the femoropatellar joint (e) can be used by passing the needle through the lateral femoropatellar ligament.

proximally, until joint fluid is obtained or the needle tip contacts articular cartilage of the distal femur (see Figure 10-25). The clinician does not need to angle the needle sharply proximally using this technique. What is sometimes frustrating is that even in horses with obvious femoropatellar effusion, a steady flow of synovial fluid cannot be obtained, and attempting aspiration of fluid with a syringe is seldom helpful, because synovial villi readily plug the needle, making aspiration impossible. Some clinicians perform femoropatellar arthrocentesis with the limb in a non–weight-bearing position, in which case a 9-cm spinal needle is used and the needle is directed proximally, between the patella and distal aspect of the femur. An alternative lateral approach to the femoropatellar joint has been described.67 An 18-gauge, 4-cm needle is inserted into the lateral cul-de-sac of the femoropatellar compartment, located about 5 cm proximal to the lateral tibial plateau, caudal to the lateral patellar ligament and the lateral trochlear ridge of the femur. The needle is directed per­ pendicular to the long axis of the femur until bone is contacted (about 1.5 to 2 cm in most horses) and then is withdrawn slightly until synovial fluid is collected.

Proposed advantages of this approach are a reduced potential for iatrogenic injury to the articular cartilage and more reliable recovery of synovial fluid compared with the subpatellar approach.68

Coxofemoral (Hip) Joint

Although the coxofemoral joint is relatively large and the landmarks for needle insertion are consistent, injection is considered to be a daunting task. Few of us perform this injection technique on a regular basis, and depth of penetration makes accurate needle placement difficult. An 18-gauge, 15-cm (6-inch) spinal needle is adequate for all but the largest of draft horses. A needle of this length should be inserted carefully, and if the horse is moving or fractious, it may be necessary to provide sedation. The site is in the angle formed between the long caudal and short cranial processes of the greater trochanter of the femur (Figures 10-26 and 10-27). This site can be difficult to palpate in heavily muscled horses, and ultrasonographic evaluation can be useful to identify the injection site. The most difficult landmark to palpate consistently, but an important one nonetheless, is the cranial process. The site

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Joint capsule (cut)

Sciatic nerve

Cranial process of greater trochanter

a Caudal process of greater trochanter Sciatic nerve

a Gluteus medius muscle

b

Greater trochanter of femur

Fig. 10-26  •  Lateral and dorsal (inset) views of the left coxofemoral joint. Arthrocentesis of the coxofemoral joint is performed by inserting the needle (a) in the angle formed between the caudal and cranial processes of the greater trochanter of the femur. The needle is inserted slightly cranially, distally, and medially just dorsal to the shaft of the femoral neck (inset). This view (b) shows the seldom used diagnostic technique of synoviocentesis of the trochanteric bursa.

Fig. 10-27  •  Arthrocentesis of the right coxofemoral joint. Using an extension set between needle and syringe, a technique that reduces the amount of manipulation necessary during the procedure, facilitates arthrocentesis of this and other joints.

is between the two processes, closer to the cranial process and not caudal to the trochanter. Before the needle is inserted, blocking the injection site may be useful. Because the shaft of the needle is handled, sterile gloves are recommended. Needle direction is important. The needle is inserted in a slightly craniomedial direction and slightly distally and directed just dorsal to the femoral neck, until the joint capsule is penetrated. In most horses, a subtle pop can be felt as this occurs. “Walking” the needle off the femoral neck may be useful, using the bone as a guide to the coxofemoral joint. In most adult light-breed horses, this occurs within 3 to 5 cm of the hub of the needle. Synovial fluid is reliably retrieved from the coxofemoral joint, spontaneously or by aspiration. A large volume of local anesthetic solution should not be injected if synovial fluid is not readily obtained, but injecting a small volume and attempting retrieval with a syringe is useful. It is possible inadvertently to inject local anesthetic solution around the sciatic nerve, causing temporary paresis, if the needle is caudally malpositioned, and therefore local anesthetic solution should not be injected if any doubt exists that the needle is correctly positioned. The amount of local anesthetic solution used is 25 to 30 mL.

Most horses are evaluated in 20 to 30 minutes, but in horses with fractures of the acetabulum the clinician should expect only 50% improvement in lameness score, and improvement may be short-lasting (15 to 30 minutes). An alternative ultrasound-guided technique has been described and is particularly valuable in large overweight horses in which the landmarks are difficult to palpate.69

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Analgesia of the navicular bursa and DFTS in the hindlimb is the same as in the forelimb.

gastrocnemius or SDFT at this level, and osseous lesions of the tuber calcanei. The bursa is located between the SDFT and tuber calcanei. Proximal to the tuber calcanei, the bursa is interposed between the SDFT and the gastrocnemius tendon. When distended, an unusual clinical finding, the bursa is palpable as medial and lateral outpouchings just proximal to the tuber calcanei. Smaller outpouchings are often discernable just distal to the tuber calcanei but are inconsistent. The bursa can be accessed for injection at any of these outpouchings. A 20- to 22-gauge, 2.5- or 4-cm needle is used to inject 10 mL of local anesthetic solution, after retrieval of fluid for analysis if indicated. Pain may take 20 to 30 minutes to abate in horses with osseous lesions or with severe lameness.

Cunean Bursa

Trochanteric Bursa

Tarsal Sheath

LOCAL INFILTRATION IN THE FORELIMB AND HINDLIMB

ANALGESIA OF HINDLIMB BURSAE AND TENDON SHEATHS

Occasionally, injecting the cunean bursa is necessary to assess the role of the cunean bursa and tendon in horses with distal hock joint pain, to perform cunean tenectomy, or to medicate the structure. The cunean bursa is seldom the sole source of distal hock joint pain but can play a role, so analgesia or medication of this structure is sometimes combined with other injections. The cunean bursa is between the distal tarsal bones and the medial branch of the cranialis tibialis tendon (called the jack tendon or cord) but is seldom palpable (see Figure 10-24). The distal aspect of the cunean tendon is usually easily palpated, however, by starting at the distal aspect of the hock and sliding the fingertip in a proximal direction. Retrieving synovial fluid is unusual but possible, but during injection the clear outline of the bursa can be seen as it distends. A 20- to 22-gauge needle is inserted deep to the distal edge of the cunean tendon and directed in a proximal direction, and 3 to 5 mL of local anesthetic solution is injected. We prefer this approach, but alternatively the needle can be inserted perpendicular to the skin and directly through the tendon itself until bone is contacted. Analgesia of the tarsal sheath is performed to confirm the structure as a source of lameness associated with traumatic and infectious tenosynovitis (although the response may be limited in the face of infection) and various osseous lesions, such as those involving the sustentaculum tali, or unusual exostoses (osteochondroma). The tarsal sheath surrounds the DDFT from a point approximately level with the tuber calcanei and extends to a point 2 to 3 cm distal to the tarsometatarsal joint. Distention of the tarsal sheath is commonly called thoroughpin, but occasionally thoroughpin appears as fluid swelling proximal to the tarsus that does not involve the tarsal sheath. The DDFT is located medial to the calcaneus as it crosses the sustentaculum tali. The heavy tarsal retinaculum medially and the calcaneus laterally restrict outpouching of the tarsal sheath to the proximal and distal aspects. The clinician should take care to differentiate tarsal sheath effusion from distention of the plantar pouches of the tarsocrural joint. A 20-gauge, 2.5-cm needle is used to inject 10 to 15 mL of local anesthetic solution.

Calcaneal Bursa

Indications for analgesia of the calcaneal bursa include traumatic and infectious bursitis, tendonitis of the

Seldom does an indication exist to block the trochanteric bursa, although injections in this region are commonly performed to manage bursitis and muscle pain (see Chapter 47). The trochanteric bursa is located between the tendon of insertion of the gluteus accessorius muscle and the cranial process of the greater trochanter of the femur (see Figure 10-26; see also Chapter 47). In normal horses this bursa is small and likely has minimal synovial fluid. Synoviocentesis is performed using an 18- to 20-gauge, 4-cm needle, although in larger, more heavily muscled horses, a longer needle may be necessary. The needle is inserted perpendicular to the skin, directly over the cranial aspect of the greater trochanter until contact with bone is made. We have had difficulty retrieving fluid even in lame horses that have a positive response to analgesia. Generally, 5 to 10 mL of local anesthetic solution are injected until pressure is felt. If local anesthetic solution can be aspirated, the needle was likely in the bursa, but if not, the injection was likely performed in the surrounding tissues.

Local infiltration of local anesthetic solution in painful soft tissues or over painful bony swellings can be performed at any location, although some areas deserve special mention. Any localized area of pain, into which a needle can be inserted safely, is fair game for local analgesia. The clinician must be aware, however, that local infiltration may not provide total analgesia to the region, mostly because the entire nerve supply to the region cannot be blocked. Incomplete analgesia is common in horses with bony lesions, such as bucked shins, because deep pain from the cortex of the McIII is difficult if not impossible to eliminate using subcutaneous infiltration of local anesthetic solution. In most instances, perineural analgesia for this particular condition is preferred. Local infiltration is performed in many horses in lieu of perineural technique, or in horses in which perineural analgesia has localized pain to a general region, but conflicting or numerous clinical problems exist. An advantage of local infiltration is that proprioception is not lost, and horses can be moved at speed for reevaluation after this form of analgesia. Efficacy can be assessed by deep, direct digital palpation, to confirm that the previously identified source of pain was eliminated by local analgesia.

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PART I  Diagnosis of Lameness

Splints

A common suspected cause of lameness in many horses are exostoses associated most commonly with the second (McII) and fourth (McIV) metacarpal bones or the MtII or MtIV, or in combination with the McIII or MtIII. A 20- to 22-gauge, 2.5- to 4-cm needle is used to deposit 5 mL of local anesthetic solution subcutaneously over the painful exostosis. The needle is slid directly alongside the proliferative lesion, between skin and bone. For splints involving the McII or MtII and the McIV or MtIV, it is important to deposit local anesthetic solution abaxial and axial (between the suspensory ligament and splint bones) to the lesion. In some horses proliferative changes involve only the axial aspect of the McII, MtII, McIV, or MtIV (blind splints), and it is critical to block in this location. In others with primary proliferation between the McII or MtII, McIV or MtIV, and the McIII or MtIII, subcutaneous injection will suffice. When local anesthetic solution is infiltrated on the axial aspect of the splint bones, the palmar or plantar metacarpal or metatarsal nerves are likely blocked, making it possible to abolish pain from a more distal site and leading to misinterpretation of results. In horses with extensive adhesions between the axial aspects of the McII or MtII and the McIV or MtIV, the suspensory ligament pain may be incompletely abolished using a local infiltration technique, and the palmar or plantar nerves and palmar or plantar metacarpal or metatarsal nerves above the site may need to be blocked individually for pain to be abolished.

Suspensory Ligament Origin

Local infiltration or flooding the palmar metacarpal or plantar metatarsal regions at the origin of the suspensory ligament is often done in lieu of perineural analgesia, as described previously. This is also referred to by some as a subtarsal or subcarpal block. An 18- to 22-gauge, 2.5- to 4-cm needle can be used to distribute 5 to 15 mL of local anesthetic solution in a fan-shaped pattern, usually from a lateral injection site just axial to the McIV or MtIV. It is important to use adequate restraint and have the limb in a flexed position when performing this technique. In the hindlimb an 18- to 19-gauge needle should be used to minimize the potential for needle breakage, should the horse kick during the procedure. False-positive results, attributed to inadvertent analgesia of palmar metacarpal or plantar metatarsal nerves, penetration of the distal outpouchings of the carpometacarpal and tarsometatarsal joints, or penetration of the tarsal sheath can occur.25,56 Compared with high palmar analgesia, the incidence of inadvertent injection of the distal palmar outpouchings of the carpometacarpal joint was highest when local infiltration of the suspensory origin was performed.25 A single injection technique was recently developed for diagnostic analgesia of the suspensory ligament origin in the hindlimb that should both limit the incidence of the previously mentioned complication, and also may be more specific for pain originating from the origin of the suspensory ligament. The technique involves blocking the deep branch of the lateral plantar nerve. The clinician holds the limb with the stifle and tarsus at 90 degrees of flexion and with the digit fully flexed. While the SDFT is deflected medially, a 2.5-cm needle is inserted to the hub, perpendicular to the skin, at a site 15 mm distal to the proximal aspect of the MtIV on the plantarolateral aspect of the limb. The

needle is advanced between the lateral aspect of the SDFT and MtIV, at which point local anesthetic solution is injected.70 It is important to understand that from the deep branch of the lateral plantar nerve originate the lateral and medial plantar metatarsal nerves that continue distally, axial to the MtIV and MtII, to provide important innervation to the fetlock joint (see previous discussion). Failure to eliminate fetlock region pain by first performing low plantar analgesia could lead to erroneous interpretation of the results of analgesia of the deep branch of the lateral plantar nerve. If only the deep branch of the lateral plantar nerve is blocked, a diagnosis of proximal plantar metatarsal pain could be made even though fetlock region pain could be the true source of pain causing lameness.

Curb

Curb, the term used for swelling of the distal, plantar aspect of the tarsus, is a complex condition involving SDF tendonitis, long plantar desmitis, subcutaneous swelling, or various combinations of these soft tissue injuries (see Chapter 78). Local infiltration can partially abolish pain associated with curb and usually involves depositing local anesthetic solution subcutaneously. Completely blocking deep pain associated with the long plantar ligament or SDFT is not possible without using the fibular and tibial nerve blocks. A tibial nerve block may be more specific.5 A 20-gauge, 2.5- to 4-cm needle is used to inject 15 to 20 mL of local anesthetic solution with the limb in a flexed position. Adequate restraint and the help of an assistant are mandatory. Local anesthetic solution is infiltrated subcutaneously along the plantar, medial, and lateral aspects of the swelling, but deep injection into or between the SDFT and long plantar ligament is avoided. The medial injection is most comfortably and safely performed by standing on the opposite side of the horse.

Dorsal Spinous Process Impingement

Infiltration of local anesthetic solution around impinging dorsal spinous processes is a technique that is performed when attempting to confirm or rule out lameness or poor performance associated with back pain caused by impingement or other pain originating from the dorsal spinous processes of the thoracolumbar vertebrae.71 The horse is usually evaluated under saddle or in harness or on a lunge line, because lameness associated with this condition may be subtle and only manifested under these conditions. The hair along the dorsal midline is clipped, and the site or sites are prepared aseptically. We prefer to use 22-gauge, 9-cm spinal needles, although in most instances shorter needles can easily reach the tops of the dorsal spinous processes. Needles are inserted on the dorsal midline and directed ventrally to the dorsal spinous processes or the interspinous space. Markers placed after scintigraphic or radiographic examination are helpful to determine the precise location for blocking or to administer medication. The interspinous space can be located by redirecting the needle in a cranial or caudal direction. If impingement of the dorsal spinous processes exists, it may be impossible to infiltrate between them, but placing local anesthetic solution around the processes is satisfactory.5 Seven to 10 mL (per site) of local anesthetic solution are deposited as the needle is slowly withdrawn, and the horse is reevaluated 10 to 15 minutes later.



Video available at www.rossanddyson.com

Using ultrasound guidance, intraarticular or periarticular injections of the cervical, thoracic, or lumbar facet joints can be performed using a 9-cm spinal needle. Injection techniques for the sacroiliac joints are described in Chapters 50 and 51.

Orthopedic Implants

Occasionally, pain associated with orthopedic implants is suspected to cause lameness. This is most commonly seen in horses after distal McIII or MtIII condylar fracture repair but can occur after repair of proximal phalanx or olecranon

Chapter 11  Neurological Examination

135

process fractures. Low-grade lameness is most common. Differentiating pain arising from negative interaction of implants with bone or surrounding soft tissue is nearly impossible based on the results of any diagnostic analgesia technique, because innervation to the joint or surrounding tissues is complex. Local anesthetic solution can be injected around screw heads, next to pins and wires or bone plates, and the horse is then reevaluated. Because lameness is often subtle, improvement is often difficult to judge. A combination of clinical findings and those from ancillary diagnostic techniques is used to determine the role of implant pain.

Chapter 101  Bone Biomarkers



101 

Chapter

Bone Biomarkers Joanna Price

References on page 1338

Bone is a complex tissue that undergoes change throughout life by the processes of bone formation by osteoblasts and bone resorption by osteoclasts.1 Modeling and subsequent remodeling of bone are required for bone health and allow the skeleton to respond rapidly to changes in its internal and external environment. Bone formation and resorption of bone are “coupled”2; the cycle of remodeling begins with the recruitment of osteoclasts, which attach to the bone surface and resorb the subjacent bone matrix. After osteoclasts evacuate a resorption pit, osteoblasts differentiate from mesenchymal precursors and fill in the lacuna with new bone matrix.3 In a healthy adult skeleton, formation and resorption are balanced. However, the balance is changed during growth, in response to altered exercise, by hormonal changes, during ageing, after therapeutic intervention, in metabolic bone disease, in neoplasia, and in response to injuries such as stress fractures.4-6 Changes in subchondral bone metabolism are also potentially important in the pathogenesis of osteoarthritis (OA).7,8 A challenge is to develop sensitive and specific noninvasive methods to detect changes in bone turnover in vivo. Abbreviations used in this chapter are summarized in Box 101-1. Changes in bone mass and structure are assessed using techniques such as quantitative ultrasound (QUS), dual energy x-ray absorbiometry (DEXA), and quantitative computed tomography (QCT).9-11 However, it may take several months for changes in bone mass and architecture to be of a sufficient magnitude to be detected with these methods. Furthermore, QCT and DEXA are not straightforward to use in a conscious horse, and use is restricted to ex vivo or in vivo research studies. Magnetic resonance imaging (MRI) is being used increasingly to study bone pathology in people,12 but in a standing horse it can be used only for the distal aspect of the limb. It is expensive and not appropriate for screening potentially at-risk populations. In contrast, bone biomarkers measure dynamic changes in bone cell activity and can be measured in body fluids using relatively inexpensive straightforward methods. Biomarker measurements can be repeated at frequent intervals and so are convenient to use in the field. Although bone biomarkers remain predominantly research tools, considerable investigation has been undertaken on potential clinical applications. Soon it is highly likely that selected biomarkers will be used in conjunction with other tools to identify at-risk horses.13,14 Ideally, a biomarker should be measurable in body fluids by a sensitive and specific technique and be specific to its tissue of origin. Detailed molecular characterization of bone has led to the development of biomarkers with

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increased specificity. Progress in equine bone biomarker research has been led by work in people—in particular, use of biomarkers to detect osteoporosis.15-17 There are a number of equine-specific assays, but most assays in use were originally developed for people. Bone biomarkers are generally classified as markers of bone formation or markers of bone resorption or degradation, although some reflect changes in both processes (Tables 101-1 and 101-2). In general, bone biomarkers are enzymes expressed by osteoblasts or osteoclasts or organic components released during the synthesis and resorption of bone matrix.15-17 However, many bone biomarkers are present in tissues other than bone and may therefore be influenced by other physiological processes. Because each biomarker may reflect a different physiological process, it is preferable to assay for a combination of markers, as this will provide more information on bone (re)modeling. However, human studies have shown that in certain diseases individual markers give more useful information than others,15 and the same may be true in horses. Other criteria that determine the value of any biochemical marker are whether the factors that control its synthesis and metabolic pathway are understood and what factors influence its biological variability. For many biomarkers used in human clinical studies, surprisingly little is known about the regulation of synthesis and metabolism, and in horses even less is understood about these variables.

BOX 101-1 

Abbreviations ALP BALP BGP BMD CTX DEXA DMD DPD GGHyl Ghyl HPLC Hyp ICTP/CTX-MMP IGF-1 IRMA MRI NTX OA OCa PICP PINP PYR QCT QUS RIA WGL

Alkaline phosphatase Bone-specific alkaline phosphatase Bone gla-protein Bone mineral density Type I collagen C-terminal telopeptide Dual-energy x-ray absorbiometry Dorsal metacarpal disease Deoxypyridinoline Glucosylgalactosylhydroxylysine Galactosylhydroxylysine High-performance liquid chromatography Hydroxyproline Carboxy-terminal cross-linked telopeptide of type I collagen Insulin-like growth factor 1 Immunoradiometric assay Magnetic resonance imaging Type I collagen N-terminal telopeptide Osteoarthritis Osteocalcin Carboxy-terminal propeptide of type I collagen Amino-terminal propeptide of type I collagen Pyridinoline Quantitative computed tomography Quantitative ultrasound Radioimmunoassay Wheat germ lectin

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TABLE 101-1 

Bone Formation Biomarkers BIOMARKER

METHODS USED

BODY FLUID

SOURCE

COMMENTS

Bone-specific alkaline phosphatase (BALP) Osteocalcin

ELISA

Serum SF Serum SF Serum SF

Bone

Some cross-reactivity with liver ALP?

Bone

Specific osteoblast product

Type I collagen

May be contribution from tissues other than bone

Type I collagen propeptide (PICP)

RIA ELISA RIA ELISA

ALP, Alkaline phosphatase; ELISA, enzyme-linked immunosorbent assay; RIA, radioimmunoassay; SF, synovial fluid.

TABLE 101-2 

Bone Resorption Biomarkers MARKER

METHODS USED

BODY FLUID

SOURCE

COMMENTS

Deoxypyridinoline (DPD)

HPLC ELISA RIA

Urine Serum Serum

Mature collagen in bone and dentin Type I collagen

Good specificity

ELISA ECLA

Urine Serum SF Serum SF

Type I collagen

May be contribution from tissues other than bone

Type I collagen

May be contribution from tissues other than bone

Carboxy-terminal cross-linked telopeptide of type I collagen (ICTP, CTX-MMP) Carboxy-terminal cross-linking telopeptide of type I collagen (CTX-I) Collagen I (Col 1)

Indirect determination by subtracting Col CEQ from C1, 2C (both measured by ELISA)

May be contribution from tissues other than bone

ECLA, Electrochemiluminescence assay; ELISA, enzyme-linked immunosorbent assay; HPLC, high-performance liquid chromatography; RIA, radioimmunoassay; SF, synovial fluid.

Bone formation biomarkers are synthesized by osteoblasts and reflect different aspects of osteoblast activity. They are all measured in serum or plasma (see Table 101-1).

adults.22 The observation that ALP activity in subchondral bone is increased in equine osteochondrosis23 provided the first indication that BALP may be a useful marker for analyzing changes in subchondral bone associated with equine joint disease (BALP as a potential biomarker for joint disease is discussed in a later section).

Bone-Specific Alkaline Phosphatase

Osteocalcin

BIOMARKERS THAT REFLECT CHANGES IN BONE FORMATION

Alkaline phosphatase (ALP) is associated with the plasma membrane of osteoblasts and is required for osteoid formation and matrix mineralization.18 Total serum ALP is derived from numerous sources and is not a specific marker of bone formation. However, because posttranslational modifications of tissue-specific ALP (which encodes bone, liver, and kidney isoforms of ALP) occur, different methods have been developed that enable separation and quantification of these isoforms. Although numerous techniques exist to characterize equine ALP isoenzymes, electrophoresis and precipitation of bone-specific ALP (BALP) with wheat germ lectin (WGL) are used most commonly.19,20 The WGL assay is more specific than a human immunoradiometric (IRMA) assay, which shows some cross-reactivity with liver ALP in horses.19 However, other, more userfriendly human immunoassays have now been validated for use in horses.21 BALP predominates in serum during growth, and this is reflected in the high concentrations of BALP measured in young horses, although the proportion of the bone isoform decreases to approximately 50% in

Osteocalcin (OCa), which is otherwise known as bone glaprotein (BGP) is the most abundant noncollagenous protein in bone matrix, and a small fraction is released into the circulation after synthesis by osteoblasts. The only other cells to express OCa protein are odontoblasts and hypertrophic chondrocytes, so OCa has tissue specificity, and it has been widely used as a sensitive and specific marker of osteoblast function in human clinical studies. Numerous studies have described the measurement of OCa in horses and the factors that influence OCa levels.24-27 Several methods have been used to measure OCa in horses, and a number of equine-specific assays have been developed; recently I used a competitive human immunoassay that has been validated for equine use.28 OCa is highly labile; therefore samples should be processed rapidly (within 90 minutes). For OCa assays, equine serum can be stored at −20° C for up to 26 weeks, although long-term storage should be below −25° C.29 OCa levels are affected by general anesthesia; therefore sampling during surgery may give misleading results.30

Chapter 101  Bone Biomarkers



The Carboxy-Terminal Propeptide of Type I Collagen

Type I collagen is the most abundant collagen in bone, and the procollagen molecule contains both amino (PINP) and carboxy-terminal (PICP) extension domains, which are split off before fibril formation and released into the circulation. These propeptides provide quantitative measures of newly synthesized type I collagen, and in people serum levels reflect the rate of bone formation. PICP can be measured in horses by human radioimmunoassay (RIA).31 However, type I collagen is not bone specific, and synthesis in other soft tissues may contribute to PICP concentrations in serum. For example, increased levels have been observed after tendon injury,32 and there is a peak in PICP levels during rapid weight gain in growing Thoroughbreds (TBs).33 Unfortunately, the human PINP assays that I have tested to date do not appear to show species cross-reactivity.

BIOMARKERS THAT MEASURE CHANGES IN BONE RESORPTION The majority of bone biomarkers that reflect osteoclastic resorption of bone matrix are degradation products of type I collagen (see Table 101-2). Originally, collagen-related resorption biomarkers were measured in urine samples collected over a 24-hour period, but in practice this is difficult in the horse. More recently developed resorption markers can be measured in serum and synovial fluid.

Cross-Linked Collagen Telopeptides

Cross-links are located at the amino (N-) and carboxy (C-) termini in the type I collagen molecule, and a number of peptide assays have been developed for measuring telopeptides generated during osteoclastic resorption. The first of these was a RIA for the carboxy-terminal telopeptide of type I collagen (ICTP), which works well for serum of the horse. Because the enzyme cathepsin K cleaves the telopeptide, the assay is now abbreviated to CTX-MMP.16 I and others used ICTP quite extensively in early bone biomarker studies in horses.31,33-35 More recently an immunoassay (CTX) was developed that recognizes ICTP containing an isoaspartyl peptide bond36 and has been used increasingly in equine studies.37,38 In people, CTX has been widely used to monitor changes in bone remodeling in osteoporosis and in joint disease,15,37 although concentrations are affected by diet.

Other Biomarkers of Bone Resorption

A number of other biomarkers have been used to monitor bone resorption in the horse, including hydroxyproline (Hyp), hydroxylysine glycosides, and the pyridinium crosslinks of collagen.39-42 Pyridinoline (PYD) or hydroxylysyl pyridinoline (HP) is found in cartilage, bone, ligaments, and vessels, whereas deoxypyridinoline (DPD) or lysyl pyridinoline (LP) is found almost exclusively in bone and dentin.43 During osteoclastic resorption the cross-links are cleaved and the components released into the circulation. Pyridinium cross-link concentrations measured in serum and urine are mainly derived from bone, and for many years urinary DPD, measured by high-performance liquid chromatography (HPLC), was considered the gold standard of resorption markers in human clinical research. HPLC

949

also provides a reliable method for measuring total urinary DPD and PYD concentrations in the horse. There are agerelated decreases in PYD and DPD levels and a significant diurnal pattern in excretion.44 In a study of acute tendon injury, urine PYD and DPD concentrations were increased, which probably reflects increased bone resorption associated with disuse.40 I have used HPLC to measure DPD and PYD in horse serum, but this assay can be used reliably only in horses younger than 2 years of age, because serum concentrations in skeletally mature horses are below the limit of detection.41 A human immunoassay was used to measure the free fraction of equine urinary DPD, and this assay can be adapted for the measurement of serum DPD.45,46 Type I collagen degradation can also be determined indirectly by subtracting concentrations of a specific type II collagen degradation biomarker, Co1 234CEQ,47 from concentrations of a biomarker that measures degradation of both type II and type I collagen (originally called COL2-3/4Cshort, now referred to ascC1,2C).48

FACTORS THAT INFLUENCE BIOCHEMICAL MARKERS OF BONE CELL ACTIVITY IN HORSES Because bone markers reflect instantaneous changes in bone cell activity, a large number of factors can be a source of preanalytical variability—controllable factors (e.g., food intake, circadian changes, or exercise) and uncontrollable factors (e.g., gender, age, or intercurrent disease).49 A failure to define and appropriately manipulate controllable sources of variability and to account for uncontrollable variability limits interpretation of the results of bone marker measurements in clinical studies. Fortunately, the analytical variability of the assays is low if carried out by a specialist laboratory.

Circadian Variability

Human studies have shown that circadian variability may have a significant effect on markers of bone turnover, particularly urinary markers of bone resorption.49 These circadian rhythms can be affected by age, disease, fasting, and drugs. Circadian rhythms in urinary PYD and DPD excretion have been described in adult geldings with peak levels occurring between 02.00 and 08.00—a pattern of change similar to that described in people.40 In a study of six 2-yearold TB mares, changes in three bone biomarkers (OCa, ICTP, and PICP) and insulin-like growth factor 1 (IGF-1) were measured over a 24-hour period. There was a significant circadian rhythm for OCa (estimated peak at 09:00) and IGF-1 (estimated peak at 17:30) but no significant circadian rhythm for PICP or ICTP.50 Others had previously described circadian rhythmicity in OCa levels in horses of different ages, although this remains somewhat controversial.25,40,51 Light may also influence OCa concentrations.25 No circadian variability in CTX concentrations was found.51 I recommend collecting samples at a similar time of day, preferably first thing in the morning before exercise.

Diet

Human studies have shown that fasting significantly reduces the circadian variation in serum levels of CTX.52 To date, no effect of feeding on bone biomarkers has been described. Little is known about the influence of diet on bone turnover markers in horses; no short-term effect on

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PART X  Lameness in the Sports Horse

OCa concentrations was found after feeding.25 Calcium supplementation has been found to suppress bone turnover in women.53 Dietary mineral supplements, widely used in horses, may influence bone markers.

Seasonal Changes

Time of year may influence bone turnover in horses, and this may be particularly important during growth. Monthly variability in ALP and OCa concentrations has been found in Finnhorse foals54; bone turnover markers in TB yearlings have been found to increase between midwinter and early summer.33 A similar seasonal pattern of change in OCa was seen in a longitudinal study of 30 Ardenner horses from approximately 1 to 2 years of age.37 CTX-I concentrations are also affected by season, with levels reaching a nadir in November before rising from November to April. In TBs the influence of season on bone biomarkers declines with age. Bone biomarkers were measured every month in more than 100 2-year-old TBs, and season did not have a significant effect on OCa, PICP, or ICTP concentrations.34

Age

In horses, as in people, bone biomarkers are higher during skeletal growth than in adults. I do not know if bone turnover increases in old horses as it does in people. An inverse relationship with age was described for several bone biomarkers in different horse breeds including OCa,* BALP,19,22,31 PICP, ICTP,33,34,56 PYD, and DPD.44 The decrease in bone turnover markers is most substantial during the first year of life, but levels do not plateau until 3 to 4 years of age. Comparison of ICTP, PICP, and OCa changes with age in early- and late-born foals showed that age-related decreases in these biomarkers were more distinct in lateborn foals,56 indicating a difference in the rate of skeletal development in foals born at different times of year. This may reflect increased activity in late-born foals that were turned out to pasture immediately after birth, whereas early-born foals were initially kept confined. Generally, biomarkers of bone formation and bone resorption have a similar pattern of change, because bone remodeling involves resorption of bone at some sites (e.g., the endosteum) and formation at others (e.g., periosteal surfaces and the metaphyses). However, an age-related decrease in CTX-I concentrations is not observed. There was no effect of age on CTX-I concentrations in 30 Ardenner horses 1 to 2 years of age37; however, levels increased at 2 to 52 weeks of age.38,57 These results call into question the bone specificity and thus the value of this biomarker in the horse. Any study of bone biomarkers must control for the effects of age, especially in young horses. Serial marker measurements (i.e., use of the horse as its own control) are likely to be most informative in young horses. Ideally each laboratory should establish its own reference ranges for each marker in horses of different ages. Published reference ranges are of questionable value because absolute levels of these biomarkers vary significantly among laboratories.

Gender

In people there are gender differences in bone biomarkers, and these vary with age.49 In horses this may depend on the specific biomarker and/or the horse’s age. There were *References 24, 26, 37, 38, 55, 56.

higher OCa levels in TB fillies of 24 to 36 months of age, but no gender difference was observed in younger horses.55 There was no effect of gender on OCa and CTX-I concentrations,37 on OCa concentration in Standardbreds of different ages,24 or on OCa or ICTP concentrations in Warmblood or draft horses older than 4 years of age.26 However, in a longitudinal study of 2-year-old TBs in race training in the United Kingdom (84 colts and 63 fillies), ICTP and OCa concentrations were higher in colts than in fillies, but there was no gender difference in PICP concentrations.34 Lower biomarker concentrations in fillies may reflect smaller bone size and/or earlier sexual maturation.

Pregnancy, Lactation, and the Estrous Cycle

The calcium requirements during pregnancy and lactation are met, at least in part, by changes in maternal bone turnover, and in people an increase in markers of bone resorption precedes an increase in markers of bone formation.58 Although not extensively studied in horses, OCa levels were unchanged in Selle Francais mares during the first 5 months after birth.59 Bone cell activity in people is regulated by sex hormones.60 In horses both OCa and ICTP concentrations were higher during the luteal phase of estrus,61 which is consistent with lower estrogen concentrations being associated with increased bone turnover. The stage of estrus must be considered as a potential source of uncontrollable variability in bone biomarker concentrations in horses as in people.49

Breed

Ethnic differences in bone turnover have been described in people,49 and horse type must also be considered as a potential effect on bone markers. The concentrations of OCa were lower and ICTP levels higher in draft horses compared with Warmbloods26, which may relate to different rates of bone remodeling. This is not surprising considering the wide variation in skeletal size between different types of horse.

Intercurrent Disease

Little is known about the effect of different diseases on equine bone biomarkers. Any condition that affects bone metabolism (e.g., nutritional hyperparathyroidism) or marker clearance (e.g., kidney disease) will influence marker concentration. Liver disease may lead to increased crossreactivity of BALP assays with the liver isoform of ALP. Fortunately these diseases are not common in equine athletes. However, an unrelated undiagnosed disease could contribute to circulating levels of a biomarker and misinterpretation of results.

CLINICAL APPLICATIONS FOR BONE BIOMARKERS Bone biomarkers have been used in human medicine to study metabolic bone disease, particularly postmenopausal osteoporosis,16,17 for prediction of fracture risk and bone loss, and for monitoring the effects of therapy.62-64 The most valuable clinical applications for bone biomarkers in the horse, particularly if measured serially in the same horse, will be for identification of horses at risk of injury or for monitoring the effects of treatment. An important research application is to monitor the effects of exercise on

the equine skeleton. However, because bone biomarkers reflect turnover in the whole skeleton and are affected by numerous variables there will always be an overlap between marker levels in normal and affected horses. Thus, in my opinion, it is unlikely that any bone biomarker measured as a “one off” will be able to function as a diagnostic test with a high level of discriminatory power.

Bone Biomarkers and Fracture

In order to assess bone biomarkers as predictors of risk of fracture (or any other condition), prospective studies are required that relate baseline bone biomarker levels to subsequent risk of injury. Bone biomarkers can be used to predict osteoporotic fracture in people.62,63 In a prospective study bone biomarkers (ICTP, PICP, CTX-I, and OCa) were measured at the start of the training season in more than 500 2-year-old and more than 300 3-year-old flat racehorses to determine if fracture could be predicted in the subsequent training season.65 The incidence of fracture was 11.6% (60 horses) but the bone biomarkers measured were unable to identify horses that sustained a fracture. Measurement of bone biomarkers longitudinally (monthly) in flat racehorses in training also failed to demonstrate a relationship between biomarkers and fracture.66 However, a field study of horses in training undertaken in the United States showed a relationship between biomarkers and injury risk.67 Whether bone biomarkers have better predictive value in older horses when the biological variability associated with skeletal growth is reduced remains to be determined.

Bone Biomarkers and Dorsal Metacarpal Disease

Dorsal metacarpal disease (DMD) is a common problem in young racehorses associated with accumulated distance trained at canter and high speed.68 In a study of 165 2-yearold TBs in training it was demonstrated that bone biomarkers measured at the start of training may have value for identifying horses at risk of developing DMD in the subsequent training and racing season.69 OCa, PICP, and ICTP were measured in November to early December, and training and veterinary records monitored for the next 10 months. OCa and ICTP were significantly higher in horses that subsequently developed DMD (horses with DMD were defined as having an episode where clinical signs of DMD were sufficiently severe for a horse to miss 5 consecutive days of training). A multivariable logistic regression model indicated that horses with ICTP concentrations above 12,365 mcg/L and older than 20.5 months are 2.6 times more likely to develop DMD.

Bone Biomarkers and Osteochondrosis

Several studies have used biomarkers to identify young growing horses which have, or are at risk of, developing developmental orthopedic disease (DOD), osteochondrosis in particular. Osteochondrosis is associated with changes in bone as well as cartilage70 and so it is appropriate to study both bone and cartilage biomarkers in the context of this condition. A small cross-sectional study demonstrated that ICTP concentrations were elevated in DOD, indicating that this disease is associated with increased bone resorption.71 However, in a study of Hanoverian foals there was no relationship between bone biomarker concentrations (OCa, ICTP, and PICP) and predisposition

Chapter 101  Bone Biomarkers

951

to develop osteochondrosis,56 although this study did not grade the severity of osteochondrosis. In contrast, there was a relationship between OCa concentrations and severity of osteochondrosis at 5 months in Dutch Warmblood foals.72 There was also a significant correlation between OCa concentrations at 2 weeks of age and the number of osteochondrosis lesions detected radiologically at 5.5 and 11 months,38 although there was no significant relationship between CTX-I and radiological status. OCa concentration at 2 weeks of age was also significantly related to necropsy score in hindlimb joints. Further studies in larger populations are required to confirm whether OCa, together with specific cartilage biomarkers, provide a reliable clinical tool for identifying young horses at risk of developing osteochondrosis.

Bone Biomarkers and Osteoarthritis

A substantial amount of research has been directed at the value of biomarkers for assessing cartilage and bone anabolism and catabolism in equine OA.73 The relationship between biomarkers of bone degradation and synthesis is reviewed because subchondral bone plays an important role in the pathogenesis of traumatic joint disease.74 BALP is a potentially useful marker for analyzing changes in subchondral bone in equine OA. ALP activity in subchondral bone is increased in equine osteochondrosis.23 In a cross-sectional study of OA, synovial fluid concentrations of BALP were significantly correlated with levels of two cartilage biomarkers and the degree of joint damage identified by arthroscopy.75 In TB racehorses with osteochondral injuries in the fetlock joints, BALP concentrations in serum were significantly lower than in unaffected controls.21 BALP concentrations were significantly higher in synovial fluid from affected carpal joints compared with normal joints. Concentrations of BALP in serum with less than 30 U/L and more than 22 U/L and a ratio of synovial fluid to serum BALP greater than 0.5 were predictive of osteochondral injury. OCa also reflects bone anabolism but was not useful in detecting early subchondral bone disease in exercised horses.76 However, a later study by the same group used a range of serum biomarkers to differentiate joint pathology and exercise-induced changes; OCa concentrations did correlate with measures of pain and modified Mankin score.77 More recently a large number of bone and cartilage biomarkers were measured in treadmill-exercised 2-year-olds with or without an experimentally induced OA lesion.78 OCa and type I collagen degradation were increased in the synovial fluid of OA joints compared with exercise-alone joints. Serum OCa and type I collagen concentrations were also significantly higher in OA-affected horses. CTX-I was not useful for separating early experimentally induced OA from exercise alone. In contrast, in human OA, CTX-I had value as a marker of bone resorption.15

EFFECTS OF EXERCISE ON BONE BIOMARKERS The responsiveness of bones to changes in mechanical load ensures that skeletal mass and architecture are sufficiently robust to prevent injury.79 Bone biomarkers provide a potentially valuable tool for studying the effect of exercise on bone and thus could possibly be used to help identify those training regimens that are osteogenic compared with

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PART X  Lameness in the Sports Horse

those that may be harmful, if the effects of exercise and disease can be distinguished.78 There are conflicting results on the effects of exercise on bone biomarkers in horses. It was suggested that a higher OCa : ICTP ratio in Warmblood horses compared with draft horses may reflect a positive modeling response in horses having regular daily work.26 Increased PICP, ICTP, and BALP concentrations have been found in treadmill-exercised 2-year-old female TBs compared with unexercised controls,80 perhaps reflecting increased remodeling from accumulated fatigue damage associated with 18 months of training on a hard surface. In contrast, a follow-up study showed that a much shorter period of training, which increased bone mineral density in the exercised group, was associated with decreased ICTP and OCa concentrations.81 A decrease in OCa was also observed when Quarter Horses commenced race training,82 and two other studies showed lower OCa concentrations at the end of a training period.83,84 In TBs in commercial race training there were decreased OCa concentrations as the intensity of work increased.66 However, OCa levels increased in young Standardbreds after 6 months of race training.85 In an experimental study designed specifically to discriminate between changes in cartilage and bone biomarkers with treadmill exercise and OA, synovial fluid and serum OCa and collagen I concentrations increased.78 There was no clear pattern of change with CTX-I, whereas a previous study in Warmblood foals found higher CTX-I levels in foals trained for the first 5 months of life compared with those raised at pasture or in a box stall.57 Changes in bone turnover may not be revealed using bone biomarkers because a training regimen is not sufficiently osteogenic. For example, lunging yearling Quarter Horses had no effect on OCa levels86; no change on DPD or OCa concentrations was observed when previously stabled Arabian horses returned to training.45 Although increased loading has anabolic effects on bone, disuse is catabolic and leads to increased resorption. Bone biomarkers have shown that a period of immobility may predispose horses to injury. When Arabian yearlings were confined to a stable, serum concentrations of the resorption marker DPD increased, whereas levels of the formation marker OCa decreased compared with levels in controls kept at pasture. There was a decrease in bone mineral content.45 A decrease in OCa levels after transfer of foals from pasture to winter stabling has been described.54 However, age and/or a horse’s previous exercise history may influence the effect of immobility on bone turnover because OCa and Hyp levels were unchanged during a 12-week period of stall confinement in older Arabian horses despite a decrease in bone mineral content.42

MONITORING RESPONSES TO THERAPY To date, monitoring responses to therapy has proved to be one of the most valuable applications of bone biomarkers in human medicine.16 The newer bone resorption markers in particular provide a very sensitive measure of the effects of antiresorptive agents on bone turnover. In osteoporotic women, type I collagen N-terminal telopeptide (NTX) and CTX decrease within months of bisphosphonate treatment.64 There is already some evidence that in horses bone biomarkers may be useful for monitoring responses to therapy and also for assessing the potentially harmful

effects of drugs on the equine skeleton. For example, bone biomarkers have showed that corticosteroids have a negative effect on osteoblast activity, and in the long term this could lead to osteoporotic changes in bone.87,88 OCa levels have been found to be significantly decreased after intravenous, intramuscular, and oral administration of dexamethasone and triamcinolone acetonide.87,88 In contrast, levels did not decrease after intraarticular injection of methylprednisolone acetate, which suggests that this route of corticosteroid administration may not have long-term adverse effects on bone.89 Serum BALP did not reflect decreased mineral apposition rate associated with phenylbutazone administration20; however, this was a relatively short-term study, and in people changes in bone formation biomarkers may not occur for several months after treatment.54 Bone marker levels were increased after growth hormone administration in horses and thus could be useful as indirect measures for detecting its abuse in racehorses.90 More recently, CTX-I and BALP were measured in a study designed to test the effect of the bisphosphonate tiludronate on disuse osteoporosis induced by the application of a cast to the left forelimb.91 There was a transient, rapid decrease in CTX-I after tiludronate administration. In my opinion the use of bone and cartilage markers to monitor the effects of treatment may be one of the most important applications for the markers in equine orthopedics, to provide an objective reflection of how treatment regimens influence catabolic and anabolic processes in bone. In conclusion, bone biomarkers provide a relatively inexpensive, straightforward, and noninvasive method for studying changes in the activity of cells responsible for forming and resorbing bone. To the basic scientist bone biomarkers can contribute to understanding the cellular mechanisms that underlie normal and abnormal bone development and (re)modeling. To the clinical researcher bone biomarkers provide insight into disease pathogenesis and assist in developing prevention and treatment strategies for equine musculoskeletal diseases. The inherent biological variability of bone biomarkers means that they are unlikely to be appropriate for diagnosing bone disease with absolute certainty when measured on a single occasion. This notwithstanding, there is accumulating evidence that bone biomarkers are potentially useful in the clinical setting, particularly when measured longitudinally with other biomarkers and used alongside diagnostic imaging modalities. Future research needs to be directed at replicating results obtained from experimental and relatively small clinical studies in large multicenter studies. There needs to be greater understanding of how variables such as exercise, growth and intercurrent disease may influence bone biomarkers, and administrators of laboratories need to start developing cost-effective, reliable biomarker panels appropriate for different clinical scenarios. If work in this area continues to progress, in 10 to 15 years bone biomarkers will likely be part of an established repertoire of tools that equine clinicians will have at their disposal for identifying horses at risk for developing disease, for achieving early diagnosis of bone and/or joint diseases, and for monitoring disease and repair progression. Inevitably this will lead to a reduction in the prevalence of lameness and wastage in equine athletes, racehorses in particular, an outcome which remains a priority and a major challenge.

Chapter

11 

Neurological Examination and Neurological Conditions Causing Gait Deficits William V. Bernard and Jill Beech

References on page 1258

Differentiating neurological gait deficits from lameness can sometimes be a dilemma for the clinician. Many repeated examinations and ancillary testing may be necessary, and even then experienced clinicians may give varied opinions about the same horse. Lack of definitive diagnostic tests to identify the origin of subtle gait changes, which in some horses may be perceived only by a rider or driver and not visible, promotes diagnoses that are based purely on opinions and individual prejudices. This chapter discusses the examination of a horse with gait deficits caused by disease of either the spinal cord, the most frequently documented cause of neurological gait deficits, or peripheral nerves. The chapter does not consider neurological syndromes characterized by signs of brain dysfunction, such as vestibular, cerebral, and cerebellar disorders. We also refer readers to a review on the equine spinal cord.1

DIAGNOSIS History is important but depends not only on asking the appropriate questions but also on many uncontrollable factors, such as how closely, impartially, and astutely the horse has been observed. The time of onset of signs and rate of progression, whether the gait deficit waxes and wanes or is affected by exercise or rest, whether one or more limbs are affected, whether the affected limb varies, what the horse was doing before onset of signs occurred, whether exercise or management has changed, whether the horse has been moved geographically, whether signs occurred after transport, what medications may have been given and any observed effects, and whether other horses

on the farm or in the stable have had any recent illnesses or fever should be determined. It is also important to know if other horses on the same farm have similar clinical signs. For instance, a history of fever, respiratory disease, or abortions in horses in contact with the affected horse would make one suspect equine herpesvirus–1 (EHV-1) infection.

Clinical Examination

The clinician should observe whether the horse displays cranial nerve dysfunction; muscle hypertrophy, atrophy, or asymmetry; muscle trembling; abnormal hoof wear; or abnormal posture. Muscle atrophy may be caused by disease of the ventral horn cells of the gray matter of the spinal cord, peripheral nerve, or the muscle itself; it also can occur with disuse. Palpation can reveal abnormalities such as altered skin temperature, sweating, muscle fasciculations, abnormal sensitivity, or soreness. The horse should be observed on a flat surface, at a walk and trot, and in straight and curving lines. The horse should be evaluated on a surface that allows detection of abnormal hoof flight and placement, toe dragging, or excessive force when landing. The sound of the feet landing should be noted for consistency and loudness. Hard surfaces also may enhance abnormal hyperflexion in horses with stringhalt. Evaluation on a soft surface may be necessary if the horse is unstable or if the clinician is trying to determine whether the horse could have sore feet. Any abnormal head or neck movement associated with limb movement should be noted. It is important to permit normal neck and head movement when the horse is being led. The person leading the horse should hold the horse as loosely as is safely possible. Collapsing or sinking on a limb, knuckling, hyperflexion, spasticity, hesitance in any part of the stride, dragging of a toe, landing excessively hard, leaning to one side, or failing to track straight can indicate a neurological deficit. Various manipulations are used to diagnose whether proprioceptive or motor deficits exist and to localize the lesion. While being led, the horse should be evaluated while stopping and starting from a walk and trot, backing up, circling tightly in both directions, walking while sideways traction is applied and released on the tail, being pushed sideways from a standstill, and walking with its head elevated. Some clinicians also evaluate repositioning of the foot after placing the horse’s hoof in an abnormal position. We do not find this particularly helpful because a horse’s disposition, age, training, and distractions can

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PART I  Diagnosis of Lameness

affect its response. A horse with a normal gait may stand with its feet placed in an abnormal position for what seems an abnormally long time. Some clinicians also use wheelbarrowing and hopping reactions.1 We do not use these tests in mature horses because we believe responses may be inconsistent and difficult to evaluate accurately and safely. Observation of the horse walking or trotting up and down inclines can be helpful in revealing whether the horse “knows where its limbs are” (proprioception) and can adjust limb movement appropriately. It may be helpful to observe the horse while it is being ridden or lunged, and in some horses while it is loose in an enclosure. Watching the horse stop and start, turn, back up, and maintain its balance during many postural maneuvers allows detection of neurological deficits that may not be obvious when the horse is being led. Consider the following: • Are errors in range of movement of the limb (dysmetria) apparent? • Is the horse extending its limbs to the full extent, or is the range decreased (hypometria)? • Does the horse lift its limbs excessively high (hypermetria)? • Is spasticity or stiffness of movement apparent? In some horses it is necessary to observe the horse performing its usual activity, providing it is capable. However, gait deficits may be much less apparent at speed than when the horse is walking or trotting slowly. Basically, the clinician is trying to determine whether the horse moves symmetrically and smoothly with normal stride length and height of foot flight appropriate to the breed and use, whether it appears strong and consistently places its feet in the appropriate positions, and whether it moves in balanced harmonious fashion. It is sometimes difficult to determine whether certain postural or gait changes are a result of pain or weakness or are associated with motor or proprioceptive deficits. Is the horse flexing its hindlimbs excessively and holding its croup more ventrally and flexed because of pain or weakness? If the horse is shifting weight between the hind feet, is it because of weakness, as seen, for example, in lower motor neuron disease, or because of pain? When both limbs are affected, manipulation of a limb to try to localize pain may not be possible. Gaited horses can be extremely difficult to evaluate, especially if one is unfamiliar with the specific gaits. Conformation also can confound interpretation of clinical signs. It may be necessary to observe the horse on many occasions and compare its gait before and after exercise. Is the deficit consistent, or does it vary? If it worsens with exercise, is it because of pain or inability to compensate for a neurological deficit as the horse tires? Perineural analgesia may be helpful. Is there palpable evidence of muscle cramping with exercise or an increase in creatine kinase (CK) level, indicating rhabdomyolysis? A variable gait deficit and inconsistent alterations in foot flight or placement are more likely to represent a neurological deficit than lameness; single limb lameness may vary in intensity but usually remains similar in character. Painful and neurological conditions could coexist but may be difficult to differentiate even with use of commonly used analgesics such as phenylbutazone. If the horse buckles in a limb, especially on turns, is easily pulled sideways by the tail when standing or walking, or trembles its limb, weakness of the extensor muscle groups should be suspected. When the flexor muscles are

weak, the horse is unable to lift its limb normally, and the toe may be worn from dragging. Pushing the horse sideways or trying to pull on the halter and tail simultaneously can reveal weakness. If the horse is weak or has pain in one limb, it is not able to bear weight normally when the contralateral hoof is lifted from the ground. Neck flexion sideways and vertically should be evaluated for ease and range of movement. Skin sensation and the cutaneous trunci reflex and cervical reflexes should be evaluated. Tapping the trunk should elicit contraction of the cutaneous trunci muscle. Abnormalities can delineate a thoracic spinal cord lesion, because afferent input is through the dorsal thoracic nerves and cranially through the spinal cord white matter, and the efferent pathway involves the cranial thoracic motor neurons in the first thoracic and eighth cervical segments and the lateral thoracic nerve. Hypalgesia of the cutaneous trunci as assessed by response to a two-pinch test with a hemostat is rare and occurs only with severe thoracic spinal cord disease.1 Lack of a cervicofacial reflex (failure of the facial muscles to twitch when the ipsilateral side of the cranial aspect of the neck is tapped) can suggest a lesion in the cervical cord or a branch of cranial nerve VII. If tapping the side of the neck fails to elicit contraction of the cutaneous coli muscle, a cervical cord lesion could exist. If any abnormal response to skin stimulation is detected, the test should be repeated because the horse’s disposition can influence its responses. Limb reflexes usually are not used, although patellar reflexes can be elicited in horses. We do not consider the thoracolaryngeal reflex (slap test) to be helpful. Response is inconsistent in horses with cervical spinal cord lesions and may be absent in normal horses. Blindfolding the horse usually is not part of our routine neurological examination unless vestibular disease is suspected. A complete physical examination should always be conducted. In some horses with hindlimb gait deficits, palpation per rectum of the pelvic bones, lumbar region, caudal aspect of the aorta, and iliac vessels may be necessary. Simple observation may not differentiate hindlimb weakness caused by spinal cord disease from that caused by partial aortoiliac thrombosis. Horses that do not “feel right” to the rider yet show no obvious deficits to the observer whether observed saddled or in hand are problematic. It may be necessary to observe a horse from a jog cart or carriage if the gait deficit about which a driver complains is not visible to the bystander. In attempting to differentiate between a musculoskeletal and neurological condition causing a gait deficit in a limb, diagnostic analgesia may be necessary. Obviously, this does not help differentiate pain from lameness emanating from a lesion proximal to the coxofemoral or scapulohumeral joints. A course of nonsteroidal antiinflammatory drugs (such as moderate doses of phenylbutazone for days or even several weeks) may be helpful in determining whether a gait deficit is caused by pain.

Hematology and Serology

In most horses serum chemistry screens and hematological tests are not particularly helpful; however, in horses with a gait deficit caused by an underlying muscle disease, evaluation of aspartate transaminase (AST) and CK levels may be helpful. Stage of training, exercise pattern, and whether the blood specimen was obtained after exercise preceded by a day of rest must be considered in evaluation



Chapter 11  Neurological Examination and Conditions Causing Gait Deficits

of enzyme levels. If a horse consistently has abnormally elevated enzyme levels, then the horse has rhabdomyolysis, and the clinician must decide whether the condition is causing or contributing to the horse’s abnormal gait. Plasma CK and AST levels do not increase simply because of muscle atrophy; rhabdomyolysis must occur to increase the enzyme levels in the blood (see Chapter 83). Elevated plasma concentrations of CK and AST in horses that are not being exercised suggest a primary muscle disorder, such as (but not limited to) polysaccharide storage myopathy (see Chapter 83). An elevation in white blood cell count and fibrinogen level indicates inflammation. In our experience, elevation in fibrinogen level is a more consistent indicator of inflammation in the adult horse than is elevation in white blood cell count. If clinical signs suggest equine lower motor neuron disease, serum levels of vitamin E (α-tocopherol) should be measured; levels of vitamin E have consistently been low in horses with confirmed equine motor neuron disease, unless the horse has been given supplements.2 Thus low vitamin E levels may be suggestive of, but are not specific for, equine lower motor neuron disease. Tocopherol concentrations can decrease during winter when horses lack access to green pasture.3 Daily variations in plasma levels may occur.4 Low levels also have been reported in clinically normal horses5-7 and in one horse with chronic gastrointestinal disease.8 The laboratory that performs the test should be contacted for any specific requirements for submission of samples and to ensure they have an established normal range for vitamin E levels. Serological testing for antibodies to various infectious agents may be indicated. In EHV-1 infection, detection of an increase in antibody titer is considered diagnostic of the disease. A horse that shows signs of neurological disease secondary to EHV-1 should have an elevated serum antibody titer, and single high titers have been the basis for initial diagnosis in individual horses. Recent vaccination confounds interpretation. Rarely, high titers may be measured in horses with no history of recent vaccination and no obvious clinical signs of EHV-1 infection. Antibody titers for Borrelia burgdorferi, the cause of Lyme disease, sometimes are measured in serum from horses with ill-defined gait deficits. High titers, or rising titers, have been used as a basis for treatment of the disease. A positive titer, however, does not mean the horse has active disease. Because of the geographical variation in exposure to B. burgdorferi, titers may vary greatly. Serological surveys in the United States have demonstrated positive test results in 1% of samples from nonendemic areas and up to 68% in endemic areas.9-11 Reports of horses “responding” to treatment exist,12,13 but to date we are unaware of any horses with Lyme disease in which neurological deficits mimic primary lameness. Currently the importance of Lyme disease as a cause of equine gait deficits is unclear. A Western blot test for the evaluation of equine protozoal myelitis (EPM) was first made commercially available at the University of Kentucky by Dr. David Granstrom.14 Serological testing for the presence of antibodies to Sarcocystis neurona can be used only to indicate exposure to the organism. Through exposure to S. neurona, many horses develop antibodies in the absence of clinical disease Serological surveys in certain areas of the United States have shown that a high percentage of horses have positive

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antibody titers. A positive test result does not mean the horse has EPM. A negative test result could theoretically occur in horses with peracute disease or perhaps in severely immunocompromised animals. However, a negative test result usually indicates that disease caused by S. neurona is highly unlikely. The test result also could be negative in a horse with signs of EPM if another protozoan, such as Neospora, causes the spinal cord lesions. In a U.S. study of several hundred horses with neurological disease, test sensitivity was 89%, but specificity was only 71%, because 30% of horses with other neurological diseases also had antibodies to S. neurona. Although the positive predictive value was only 72% in horses with neurological diseases, the negative predictive value was almost 90%, indicating that a negative test result is useful in this population.14 In one study of 44 horses on a farm sampled for more than 1 year, all horses were seropositive for at least 50 weeks yet showed no neurological signs (see following discussion).15

Cerebrospinal Fluid Aspiration and Analysis

Cerebrospinal fluid (CSF) can be obtained from either the atlantooccipital or the lumbosacral space. The advantage of lumbosacral centesis is that it can be performed in the standing sedated horse, whereas atlantooccipital centesis requires general anesthesia. Fluid from the atlantooccipital site is considered easier to obtain and not as likely to be contaminated with blood. The atlantooccipital site is identified by palpating the cranial edge of the wings of the atlas. The hair is clipped and the site prepared aseptically. Atlantooccipital centesis is performed at the intersection of the median plane and a line drawn across the cranial edge of the wings of the atlas. In an adult horse, a 9-cm (3 1 2 -inch), 18- or 20-gauge spinal needle is directed toward the horse’s lower lip with the head held in a flexed position. It is important that the needle remain on the midline as it is advanced, because otherwise it will be too far lateral to enter the subarachnoid space. The needle is initially inserted to a depth of approximately 2.5 cm (1 inch) and then gradually advanced. While the needle is gradually advanced to the subarachnoid space, it should be held carefully to prevent penetrating the spinal cord when advancing through the atlantooccipital membrane and the dura mater. Usually a “pop” is felt as the needle advances through the dura; however, this finding is not consistent and the stylette should be frequently removed to observe for flow of CSF. CSF usually flows from the needle once the subarachnoid space is entered; however, once a substantial depth has been reached (about 5 to 8 cm [2 to 3 inches] in an average-size horse), some clinicians advise gentle and frequent aspiration with a small syringe. In preparation for aspiration from the lumbosacral space the type and degree of restraint is guided by the horse’s behavior, the horse’s stability, and the clinician’s personal preference. A nose twitch, stocks, sedation, or a combination of physical and chemical restraint are options. We prefer to use light sedation with xylazine, sometimes combined with butorphanol. However, lumbosacral CSF pressure can be transiently decreased up to 15 minutes after administration of a high dose of xylazine (1.1 mg/kg intravenously).16 The puncture site for lumbosacral centesis is identified by combining several landmarks, realizing that individual variation exists. A line drawn between the caudal edge of the tubera coxae and the intersection with

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the midline can be used to locate the lumbosacral space. The lumbosacral space is bordered cranially by the caudal edge of the sixth lumbar vertebra, caudally by the cranial edge of the sacrum, and laterally by the medial rim of the tubera sacrale. The dorsal spinous process of the last lumber vertebra is lower than the dorsal spinous process of the fifth lumbar vertebra. The V formed by the medial rim of the tubera sacrale is one of the more useful landmarks, and the appropriate site for puncture is within this V. The site should be prepared aseptically, and local anesthetic solution is placed subcutaneously. A small skin stab incision is usually made. The needle is inserted on the midline, at the depression palpated just caudal to the last lumbar vertebra, in the middle of the V formed by the tubera sacrale. A 15-cm, 18-gauge spinal needle is generally adequate for a horse that is 16 hands or less. A 20-cm needle may be necessary in a horse greater than 16 to 17 hands. While the clinician advances the needle, it is critical to remain on the midline. The needle can be advanced until a pop indicates it is advancing through the dura or until the horse responds as the needle stimulates nervous tissue. These responses can be unreliable and occasionally dangerous for the horse, the handler, and the individual performing the centesis. Because horses can react unpredictably (including rearing, bolting, collapsing, or kicking), it is safer to advance the needle gradually until it is near the spinal canal, approximately 12.5 cm (5 inches) in a 15- to 16-hand horse. Once the needle is near the canal, it should be advanced slowly with repeated frequent removal of the stylette and aspiration with a small syringe. The horse may move its tail when the dura is penetrated, but usually minimal reaction occurs. If fluid is obtained but the amount is small, the needle can be rotated 180 degrees. Jugular vein compression for at least 10 seconds (Queckenstedt’s test) is thought to elevate intracranial CSF pressure and aid fluid collection, provided flow is not obstructed. If a hemorrhagic sample is thought to be from iatrogenic causes, the syringe can be changed frequently until subsequent aliquots are clear. If fluid is not obtained on the first attempt, the needle is withdrawn and the procedure is repeated slightly cranial or caudal to the original location. CSF samples should be placed in sterile tubes and rapidly processed after collection. Normal CSF is clear and colorless, and red discoloration indicates hemorrhage. However, normal fluid can sometimes appear mildly hazy when grossly examined, especially in a tube with ethylenediamine tetraacetic acid. Hemorrhage can be iatrogenic or caused by underlying disease. Fluid may appear clear even with red blood cell contamination, and studies indicate that subjective evaluation of spinal fluid is sensitive in detecting blood only when the red blood cells number more than 1200/mcL.17,18 Centrifugation of a bloody sample should produce a clear fluid with a pellet of red blood cells on the bottom of the sample tube. If hemorrhage occurred before collection and lysis of cells occurred, the supernatant may be slightly pink or xanthochromic (orange/yellow or yellow). Lysis of red blood cells reportedly can occur within 1 to 4 hours.19 Xanthochromic CSF results from red blood cell breakdown products (bilirubin) and suggests hemorrhage or vasculitis. A centrifuged xanthochromic sample does not become clear. Turbid CSF may appear with hypercellularity or epidural fat contamination. The latter is not uncommon

with lumbosacral aspirates. Formulas used to differentiate between white cell or protein elevations caused by iatrogenic blood contamination of CSF versus pathological increases have been shown to be unreliable. Contamination with a few thousand red blood cells results in minimal increase in white blood cell count or protein content.18 The normal reported range for leukocyte counts has been variable; usually a range of 0 to 6/mcL is cited,20 but higher values have been reported.21,22 Diversity in techniques can account for different values in normal CSF. Undiluted fluid can be assayed in a hemocytometer, or acidified crystal violet can be added to accentuate the cells.20 It is important that equine reference values be determined in the laboratory the practitioner uses. As previously stated, the cell quality rapidly deteriorates in CSF, and samples for cytological testing should be processed rapidly or a portion fixed in 40% ethanol if processing must be delayed. For morphological and differential evaluation, cytocentrifugation or filtration through a glass fiber membrane filter is the preferred method of processing spinal fluid. In our experience, cell and differential counts are often normal in horses with spinal cord disease. Small lymphocytes and monocytes are normally seen. Neutrophils may be seen with blood contamination or inflammation. Eosinophilia is rarely seen in equine CSF but could occur secondary to parasite migration. Rarely, eosinophils have been seen in samples from horses with protozoal encephalomyelitis,21 but frequently spinal fluid from horses with EPM is normal. A relative neutrophilia, with or without an increase in cell count, indicates inflammation, and intracellular bacteria may be seen in horses with bacterial meningitis. Reported values for protein content of CSF vary considerably among laboratories, probably because of diversity in measurement techniques. A range of 10 to 120 mg/dL is generally acceptable, although some authors consider 100 to 105 mg/dL the high end of normal range.20,23 Protein may increase because of vascular leakage (vasculitis), inflammatory lesions, trauma, iatrogenic blood contamination, or intrathecal globulin production. High-resolution protein electrophoresis of CSF has been reported in a small number of horses, but its value as a diagnostic test remains to be determined. Compared with normal horses (n = 18), horses with cervical cord compression (n = 14) often had a decreased β fraction and post-β peaks.24 However, divergent findings have been reported. Because CK is abundant in neural tissue (and in skeletal tissue and cardiac muscle) and is a large macromolecule that does not cross the bloodbrain barrier, measurement was suggested to be a sensitive index of central nervous system lesions. Horses with EPM were reported to frequently have increased CSF CK concentrations, unlike horses with cervical vertebral malformation.25 However, another study showed that the sensitivity and specificity of CSF CK activity are inadequate for diagnostic use. Also, CSF simultaneously collected from the atlantooccipital and lumbosacral sites had disparate values for CK activity, which was not associated with site or other CSF parameters. Contamination of CSF with either epidural fat or dura, which is possible during collection, increases CK activity.26 Albumin is the predominant protein in normal CSF. Elevated albumin concentration can indicate hemorrhage or altered blood-brain barrier integrity. To eliminate



Chapter 11  Neurological Examination and Conditions Causing Gait Deficits

serum albumin as a source of increased CSF protein and albumin, the following albumin quotient (AQ) has been suggested27: AQ =

CSF albumin ×100 Serum albumin

The AQ cited for normal equine CSF is 1.4 ± 0.04,23,27 and it was suggested that an increase above reference range indicated blood contamination during sample collection or compromise of the blood-brain barrier. The immunoglobulin G (IgG) index CSF IgG concentration CSF albumin concentration ÷ Serum IgG concentration Serum albumin concentration was suggested to be useful for differentiating intrathecal IgG production from an increase secondary to blood contamination or increased blood-brain barrier permeability. Normal reference range has been reported to be 0.14 to 0.24.27 However, we do not consider these to be specific, and blood contamination can increase the IgG index without a concomitant change in AQ.18 Although CSF cell count, cytological examination findings, and total protein concentration often do not represent the extent or type of spinal cord or brain tissue disease, when abnormal, the values can be useful. For example, in central nervous system (CNS) disease caused by EHV-1 infection the fluid may be xanthochromic with a high protein level but normal cell count. This disassociation between elevation in protein level and normal cell count may help differentiate EHV-1 infection from EPM. Also, xanthochromic CSF indicates an alteration in the bloodbrain barrier and could explain false-positive CSF immunoblot findings for S. neurona in a horse with positive serological test results. Unfortunately, except for EHV-1 infections and meningitis, CSF analysis with currently available tests frequently is not helpful in diagnosing spinal cord disease in horses. In the United States, the frequency of performing CSF aspiration increased with the introduction of a Western immunoblot test for detecting S. neurona antibodies. Although limited data are available, the specificity and sensitivity of the immunoblot test on CSF from horses with clinical signs consistent with EPM were reported to be approximately 90%.14 However, positive test results have been found in clinically normal horses and in horses with neuropathological lesions other than EPM. Even minute amounts of contamination of CSF with blood can cause the test result to be positive in a horse with high serum antibody levels.19 When CSF was contaminated by even minute amounts of strongly immunoreactive blood (10−3 mcL of blood per milliliter of CSF), the fluid was falsely positive even though the AQ was normal.18 This small amount of blood contamination is grossly undetectable and can correlate with as little as eight red blood cells/ mcL of CSF. Also, blood contamination, without increasing the AQ, can increase the IgG index. The IgG index is not specific for intrathecal IgG production. Although the red blood cell count may be a more sensitive indicator of blood contamination than the AQ, it does not correlate with the amount of antibody contamination. Minute amounts of highly immunoreactive blood may have a greater impact on CSF Western blot analysis than a greater amount of contamination with blood with low immunoreactivity.18

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Any compromise to the blood-brain barrier regardless of cause allows antibodies to leak into the CSF from the serum, causing a false-positive test result. Although the test for immunoblot S. neurona antibodies was reported to have 85% positive predictive value in a study of horses with neurological disease,14 in the general equine population the test has poor positive predictive value. Many normal horses have positive antibody test results.28 In contrast the negative predictive value for the test is high. With what is currently known, interpretation of positive Western blot results must be made with caution. Negative Western blot test results are generally useful to rule out EPM. Since the introduction of the original CSF Western blot analysis detecting antibodies to S. neurona, other tests have been developed. These tests include a modified Western blot, an enzyme-linked immunosorbent assay (ELISA), and an immunofluorescent antibody test. Large scale critical evaluation of these tests has not been performed. However early indications suggest that all of these tests may have some limitations. The immunofluorescent antibody test cross-reacts with Sarcocystis fayeri, therefore resulting in false-positive diagnosis of S. neurona infection.29 The ELISA is based on a surface antigen that is missing in some strains of S. neurona; therefore, false-negative results may occur.30 For the reasons discussed previously, both the original and modified Western blot tests may produce false-positive results. In conclusion, antibody testing for S. neurona infection must be used cautiously and in conjunction with other diagnostic tests in attempts to rule out other causes of neurological disease. Polymerase chain reaction (PCR) testing detects DNA of infectious organisms and has been applied to CSF. Its value in the diagnosis of EPM is controversial, especially when positive results have been reported on CSF samples that were negative for S. neurona antibodies and from horses that did not exhibit overt neurological deficits. We do not find PCR testing for the diagnosis of EPM useful. Use of the PCR technique on CSF has been helpful in diagnosing neuroborreliosis in a horse. Similar to some human cases, the PCR test result was positive yet the CSF had a negative antibody titer.12

Radiography

The use of radiographs in evaluating traumatic or infectious injuries, congenital lesions, and developmental malformations of the spinal column is limited by the size of the horse. Radiographs are useful in diagnosing congenital abnormalities of vertebrae, narrowing of intervertebral disk spaces, stenosis of the cervical spinal canal, osteoarthritic changes, osteomyelitis or osseous cysts, vertebral neoplasia, malalignment, and fractures. However, in most mature horses, except for the cervical spine, general anesthesia may be required for adequate radiographs of the spine. Computed tomography (CT) and magnetic resonance imaging have tremendous potential for evaluating the equine central nervous system but also are limited by the size of the horse. At present, except in foals, CT is available only for evaluating the head and cranial midcervical regions. The primary use of radiology in evaluating horses with neurological disease is localization of cervical vertebral lesions or cervical vertebral malformation and diagnosis of cervical compressive myelopathy or stenotic myelopathy (see Chapter 60).

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PART I  Diagnosis of Lameness

Survey radiology is useful in the diagnosis of cervical vertebral malformation and cord compression but can be misleading. Standing lateral radiographic images of the cervical vertebrae are routinely evaluated to detect vertebral malformation and to measure spinal canal diameter and can suggest the likelihood of cervical compressive myelopathy.1,31,32 In horses with cervical compressive myelopathy, malformations that characteristically may be identified include flare of the caudal epiphysis of the vertebral body (vertebral endplate modeling), caudal extension of the dorsal laminae, vertebral nonalignment, and osteoarthritis of articular facets. Modeling of the articular processes of the caudal cervical vertebrae is a common malformation identified in horses with cervical compressive myelopathy and in horses that do not have cervical compressive myelopathy. Radiological interpretation of changes is more difficult in older horses, because obvious changes may be seen, without impingement on the spinal canal. Subjective evaluation of articular facet abnormalities can result in a false-positive diagnosis of cervical compressive myelopathy. Identification of characteristic vertebral malformations supports but does not confirm the diagnosis of cervical compressive myelopathy, and subjective radiological evaluation of a malformation does not reliably differentiate between horses with or without cervical compressive myelopathy. Objective assessment of vertebral canal diameter is a more reliable indicator of cervical compressive myelopathy than the subjective evaluation of vertebral malformation. The minimum sagittal diameter (MSD) is the first described method of assessment of canal diameter based on lateral cervical radiographs.31 Determination of canal diameter using the sagittal ratio improves on the original measurements by adjusting for magnification and providing a more accurate adjustment for body size.32 The sagittal ratio measurements were developed using a population of affected (confirmed by myelogram or histopathological studies) versus nonaffected horses.32 The sagittal ratio is determined by dividing the MSD by the width of the corresponding vertebral body. Although a sagittal ratio percent at any cervical vertebra from the third to seventh cervical vertebrae less than 50% is a strong predictor of spinal cord compression, a few horses with no pathological evidence of spinal cord compression have had sagittal ratios of less than 50%. Recently intervertebral measurements of canal diameters were shown to improve diagnosis of cord compression, and addition of intervertebral sagittal ratio measurements was recommended to increase accuracy of plain radiographs.1 A semiquantitative scoring system for evaluating cervical radiographs in horses younger than 1 year of age has been published. This scoring system used neurological examination alone to determine affected versus nonaffected foals and combined subjective determination of radiographic vertebral malformation and objective determination of canal diameter.31 Vertebral canal stenosis is determined by measurement of intervertebral and intravertebral MSD. Dividing the MSD by the length of the vertebral body corrects for magnification. Malformation is determined by the subjective assessment of five cate­ gories. The most discriminating factors in the semi­ quantitative scoring system in differentiating affected from nonaffected foals are canal stenosis and the angle between adjacent vertebrae. The disadvantage of the

semiquantitative scoring system is the inclusion of subjective determinations. Myelographic examination is advised to obtain the best evidence of compression.1,33-35 Myelograms also can demonstrate compression from soft tissue masses, which are not evident radiologically, and suggest transverse compression. However, myelography may not be definitive and occasionally is misleading. A study to evaluate myelography critically and compare the results with necropsy findings in a large number of horses has not been done. A diagnosis of cord compression is assumed if a 50% reduction in the width of the dorsal dye column exists. However, the diagnostic criterion of 50% decrease in width of the dorsal dye column is not well documented34 and has been found in horses with no histological evidence of cord compression at the site of dye column decrease. Iohexol is currently the preferred contrast medium for myelography. It is important that the owner understand the advantages and disadvantages (including risks) of a myelogram before the procedure is undertaken.

Electromyography and Nerve Conduction Studies

Recording electrical activity of muscles can indicate whether evidence of denervation or a myopathy exists, although the distinction is not always clear-cut. Electromyographic examination findings in the early stages of disease or injury may be normal. Certain abnormal patterns can indicate denervation. However, depending on the specific areas to be examined, electromyography may require anesthesia or heavy sedation. It may be helpful in identifying abnormal muscles and indirectly the affected nerves. In a standing, awake horse, spontaneous muscle movement can hinder interpretation. Values for sensory and motor nerve conduction velocities in horses and ponies were reported.36-39 Differences in speed of conduction occur in different nerves and horses’ sensory nerve conduction velocities are slower than those of ponies.39 However, similar motor nerve conduction velocities were reported for the median and radial nerves of ponies and horses.37 Location of the segment being measured may be important, because distal tapering of nerves may be associated with slower velocity. Skin temperature significantly affects nerve conduction velocity,39 and variability in technique can alter findings. Slower motor nerve conduction velocities were reported in horses older than 18 years of age.36 The procedure usually requires that the horse be anesthetized and, similar to electromyography, should be performed by a skilled person. The technique mainly has been used in research.

Nuclear Scintigraphy

Nuclear scintigraphy has been helpful in identifying lesions in the cervical, thoracic, and lumbar spinal column and pelvic areas not readily evaluated by radiography. It also has been used to evaluate vertebral changes identified radiologically, to determine whether active bone change has occurred. It has revealed hairline fractures and other unsuspected bone lesions in the appendicular skeleton as the cause of gait deficits, which sometimes had been suspected to be caused by spinal cord disease. Scintigraphic imaging from both sides of the horse can differentiate which side may have a lesion. The role of nuclear scintigraphy in diagnosing equine spinal cord disease is limited.



Chapter 11  Neurological Examination and Conditions Causing Gait Deficits

Ultrasonography

Ultrasonography has been used to diagnose aortoiliac thrombosis and to identify soft tissue masses near the spine or deep within muscles. It has also revealed bony proliferation or fractures of the pelvis in horses with obscure gait deficits that were originally suspected to be a result of spinal cord disease.

Virus Isolation

If horses die or are euthanized with neurological signs thought to be caused by viral disease, the spinal cord, brain, or both should be sent for virus isolation. In horses with acute disease, nasal swabs and whole blood samples can be collected.

Immunohistochemistry and Polymerase Chain Reaction Testing

Immunohistochemistry and PCR testing can be used to detect the antigen of certain infectious organisms and are applied most commonly to tissues collected at necropsy but can also be used on affected tissues obtained by biopsy.

SPECIFIC DISEASES AND SYNDROMES Equine Protozoal Myelitis (EPM)

EPM was first reported in 197440-43 and appeared to be the same condition originally reported as segmental myelitis of unknown cause.44 It is caused by infection with S. neurona. EPM currently appears to be limited to the Western hemisphere. It is particularly of concern in the United States, where in some regions high percentages of horses are infected. The actual number of horses confirmed as having neurological disease from EPM is much lower than the actual number of horses infected, but the disease does have a substantial and serious impact. EPM has not been confirmed in horses younger than 6 months of age, although antibodies were detected in serum from a 2-month-old foal.45 A recent comprehensive review of this disease should be consulted for details.46 Neospora species have been identified as a cause of EPM in horses from the western United States.47-50 CSF testing was positive for S. neurona antibodies by Western blot test, and no antemortem features distinguished Neospora infection from Sarcocystis infection. The disease caused by S. neurona tends to occur in warm, temperate, nonarid areas with resident opossums. The horse is a “dead-end” host, and the disease is not contagious. The life cycle is not completely understood, although opossums have been identified as the definitive host. The proportion of infected horses that show clinical signs is low. This disease can cause gait deficits affecting one or all limbs and may be difficult or impossible to differentiate from musculoskeletal or other neurological diseases. Signs ascribed to EPM by veterinarians in the United States have been seen in horses in the United Kingdom, where horses have no known exposure to the organism.1 Infected horses and horses with confirmed EPM seen in Europe, Asia, or South Africa have been imported from the Western hemisphere.46 Horses frequently show asymmetrical deficits and may have focal or multifocal muscle atrophy or cranial nerve deficits. Horses may have profound or mild motor or proprioceptive gait deficits, and onset of signs can be acute or chronic, with slow or rapid progression. It may

141

be difficult or impossible to differentiate subtle neurological deficits from those caused by subtle lameness or musculoskeletal pain. Behavior may change. Focal sweating may occur. Diagnosis is based on clinical signs and history, by eliminating other potential causes by radiography and other diagnostic tests, and by testing of serum or CSF for antibodies to S. neurona. No definitive antemortem test exists, although absence of serum antibodies to S. neurona makes it highly unlikely that a horse has EPM. If a horse demonstrates classic signs (e.g., asymmetrical motor deficits and muscle atrophy in the hindlimbs, asymmetrical motor deficits in one or more limbs, a limb deficit combined with cranial nerve deficits not deemed caused by peripheral nerve trauma) and has no other organ dysfunction, we would treat the horse for EPM if it has been in the United States and serological findings are positive. We would forgo CSF testing for reasons outlined earlier. To date, drugs used to treat EPM have been a combination of trimethoprim-sulfa (sulfadiazine or sulfamethoxazole) and pyrimethamine, or sulfas and pyrimethamine, diclazuril, toltrazuril, and nitazoxanide. Because no definitive antemortem test exists to confirm the disease, evaluation of response to therapy is problematic, especially because the clinical syndrome as treated is so variable and often poorly defined. To date, no treatment trials of experimental infections have been reported. Confounding assessment of drug response is the fact that experimentally infected horses develop clinical signs that decrease over time, despite receiving no treatment.51 Numbers of organisms ingested, virulence factors, and the horse’s own immune status (which depends on heredity, previous exposure to S. neurona, stresses such as transport and parturition, lack of adequate nutrition, and other factors) all presumably can affect development of and recovery from the disease. In the United States the most widely used drug combination is one of the sulfa drugs and pyrimethamine. Because pyrimethamine reaches higher concentrations in the CSF and neural tissue, it is considered superior to trimethoprim. The usual dosage regimen is 20 mg of sulfadiazine per kilogram once or twice daily and 1 mg of pyrimethamine per kilogram once daily, both by mouth for at least 2 to 3 months. Diarrhea occasionally occurs in horses treated with trimethoprim-sulfamethoxazole, and anemia and leukopenia have been observed in some horses receiving 1 mg of pyrimethamine with sulfas per kilogram twice daily. Whether horses require such a prolonged course of treatment or continued high levels of pyrimethamine is unknown. Earlier treatment regimens used a lower dose, but to our knowledge no observations comparing dosages have been reported. A syndrome of bone marrow aplasia and hypoplasia, renal nephrosis or hypoplasia, and epithelial dysplasia was reported in three foals born from mares given sulfonamides, trimethoprim, pyrimethamine, vitamin E, and folic acid during gestation. The authors of that report suggested that administration of the folic acid reduced absorption of active folic acid and, combined with the folic acid inhibitors (trimethoprim and pyrimethamine), induced folic acid deficiency and lesions in the foals.52 We do not routinely add supplements for horses being treated with trimethoprim or pyrimethamine, but if sequential blood tests indicate anemia or leukopenia, the horse should be given folinic acid, a form of bioactive tetrahydrofolate. Folic acid should not be used because it

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PART I  Diagnosis of Lameness

is poorly absorbed in the horse, conversion to its active form is prevented by the dihydrofolate reductase inhibitors pyrimethamine and trimethoprim, and it can competitively decrease absorption of the active form of folic acid.46,52 Diclazuril, a coccidiostat, has anti–S. neurona activity in cell cultures infected with S. neurona53 and has been used to treat horses with suspected EPM.54 It is absorbed quickly after feeding. Dosage and therapeutic efficacy are being evaluated. Toltrazuril, like diclazuril, is a triazine-based anticoccidial drug. Because the drug has good lipid solubility and oral absorption and is absorbed into the CSF, it has potential for treating EPM.55 Ponazuril, a metabolite of toltrazuril, has in vitro activity against S. neurona.56 Ponazuril appeared to have favorable clinical results in a multicenter treatment study.46 The drug has undergone U.S. Food and Drug Administration (FDA) testing, has been approved, and is marketed under the trade name Marquis. Label recommended dosage is 5 mg/kg administered once per day orally. Studies have shown that Marquis has a wide range of safety. The lack of complicating side effects has led to numerous nonlabel dosage regimens. Some of these dosage regimens include double doses for the first 3 to 5 days of therapy, loading doses of 7 times the recommended dose followed by twice the recommended dose for the duration of therapy, and high doses given once weekly or monthly. These nonlabel uses have not been critically evaluated and should be used with caution. Nitazoxanide kills S. neurona in cell cultures and has been tested in a field trial. Safety studies showed lethargy at twice the recommended dose and illness and death at four times the recommended dose. Gastrointestinal upset can be a complication of nitazoxanide therapy. Concurrent administration of a vegetable oil (corn oil) with nitazoxanide appears to increase small intestinal absorption and reduce gastrointestinal upset. Manufacturers have also recommended starting therapy with a reduced dose for several days. In seven horses with clinical signs compatible with EPM and positive immunoblot results for S. neurona antibodies in the CSF, clinical signs improved in six horses by the end of the trial (85 to 140 days).57 Clinical signs recurred in two horses when treatment was stopped, but signs improved when treatment was reinitiated. Another report described two horses with a diagnosis of EPM that improved after 28 to 42 days of treatment with 50 mg of nitazoxanide per kilogram once daily.58 Anorexia and depression were reported as side effects.58 The CSF remained positive for S. neurona antibodies. Until more information is available about this drug, we do not recommend its use. Although nitazoxanide received FDA approval and was marketed as Navigator, recently the drug was taken off the market presumably as a result of gastrointestinal complications. To our knowledge, no evidence shows that concurrent use of immune stimulants, oral antioxidants, and antiinflammatory drugs has any beneficial effect. The use of corticosteroids is controversial, because some clinicians claim corticosteroid administration can exacerbate infection. Severity of neurological signs in horses infected with S. neurona reportedly was increased by corticosteroids,59 but in another study of induced disease, signs were less severe in horses given corticosteroids.60 Providing an accurate prognosis is difficult, given the inherent diagnostic problems. Some horses that recover or respond to treatment may not have EPM, and others may

recover spontaneously. Economic factors influence duration of treatment and time allowed for convalescence. Even when a severely affected horse improves dramatically, if recovery of function is not complete, a return to previous performance levels is not possible. Signs also may recur in the same horse; whether this is caused by recrudescence of infection or reinfection is unknown. We usually give a guarded prognosis for full recovery of horses showing moderate gait deficits compatible with EPM. Because the exact life cycle and natural intermediate hosts are unknown, definitive recommendations for control of the disease are difficult. Because the opossum is the definitive host and sheds sporocysts, which the horse ingests, fecal contamination of feedstuffs or water sources by this animal should be prevented. The role of other intermediate mammalian hosts is unclear. The efficacy of a recently introduced vaccine remains to be determined.

Cervical Spinal Cord Compression

Cervical vertebral malformations of various types have been described as the cause of cord compression and neurological signs.1,61,62 Occasionally it may be difficult to decide if a horse is mildly affected by cervical cord compression or is bilaterally lame in the hindlimbs. Mildly affected horses may show only a slightly stiff, stabbing gait at a walk and trot, only mild circumduction of the outside hindlimb when turning, and equivocal hindlimb dysfunction at a canter. Horses with bilateral osteochondrosis dissecans of the hocks or stifles may show similar signs but usually also have joint capsule distention. Thorough lameness and neurological examinations and radiographs are needed. With more severe compression, the gait deficits increase. Circumduction may be severe, and the horse may strike the distal aspect of the limb with the opposite hoof, causing hair loss or wounds from interference. A horse may lose balance or fall, especially when backing up or turning. If the caudal cervical spinal cord is compressed, thoracic limb motor deficits and hypometria, frequently asymmetrical, may occur. The horse may severely scuff or drag its toes and have abnormal hoof wear. Occasionally, substantial bony proliferation at the synovial articular facets can result in neck stiffness and decreased ability to turn in one direction. Cervical muscle atrophy is rare but can occur if the nerves or lower motor neurons are affected. An affected horse usually lacks hindlimb impulsion and may have a somewhat stiff, bouncy canter. The horse frequently is imprecise when stopping, and the hindquarters may sway or bounce. When compression of the cranial cervical spinal cord occurs, the horse may hold its neck and head higher than normal, in an extended position, and in horses with severe clinical signs all limbs may be affected. Signs may occur suddenly or have a more gradual onset, and progression is variable. Various vertebral abnormalities have been reported in young horses, but clinical signs can be delayed, even when radiographs reveal chronic lesions. We suspect that trauma may cause a preexisting lesion to become clinically relevant. If a horse with vertebral malformation falls, acute spinal cord compression can occur. Acute cervical spinal cord compression caused by trauma can cause tetraparesis or recumbency, but signs may be delayed in the initial stages after injury and may become apparent only when muscle spasms subside, the unstable fracture displaces,



Chapter 11  Neurological Examination and Conditions Causing Gait Deficits

or progressive hemorrhaging is present. In the neck the occipitoatlantoaxial and caudal cervical regions are predilection sites for spinal cord injury.1 Synovial cysts may also cause severe sudden signs of spinal cord compression, often asymmetrical and sometimes intermittent.1 The diagnosis of synovial cysts is usually made at necropsy. Diagnosis of cervical cord compression is based on radiography and myelography. Numerous types of vertebral abnormalities have been described. Management depends on the nature of the lesion, severity of clinical signs, intended use of the horse, and financial considerations. Horses affected by cervical vertebral malformation and cord compression at less than a year of age may improve when exercise and energy intake are restricted.63 Although no controlled studies of a paced diet and restricted exercise program have been conducted, clinical experience supports its use in young horses with radiological evidence of cervical vertebral malformation.1,63 This treatment is not helpful for young horses with very severe stenosis, for defects such as occipitoatlantoaxial or other cranial cervical malformations, or for older horses. Prognosis with conservative management is poor. Surgical fusion of vertebrae is indicated in some horses and has been used successfully.62,64,65 This subject is discussed in Chapter 60.

Equine Degenerative Myeloencephalopathy and Neuroaxonal Dystrophy

Horses mildly affected by equine degenerative myeloencephalopathy and neuroaxonal dystrophy may be misdiagnosed as being lame. Clinical signs may be somewhat similar to those of cervical spinal cord compression. Because no definitive antemortem test exists, clinical diagnosis is based on clinical signs, sometimes supported by the presence of other affected horses on the same farm or in the same family. Equine degenerative myelopathy is thought to be a vitamin E deficiency, with a likely genetic predisposition.66,67 Neuroaxonal dystrophy appears to have a genetic basis in Morgan horses.68 Various breeds and also Przewalski’s horses and zebras can be affected, and no geographical restriction is apparent. When horses are affected at a young age (i.e., 3 months) and controlled return to exercise, but they were the group most likely to do poorly or to remain lame. Horses (five) with PT-PL swelling and abscessation had surgical drainage and appropriate antimicrobial therapy and successfully returned to exercise. Associated ipsilateral lameness conditions included osteoarthritis of the centrodistal and tarsometatarsal joints and metatarsophalangeal joint pain. Curb was previously described as simply LP desmitis,1,2,5 but is a collection of plantar tarsal soft tissue injuries. In fact, in 68% of horses with curb in this study, the LPL was normal ultrasonographically, and horses with curb were more likely to have injury of the PT-PL tissue alone or in combination with SDF tendonitis than injury of the LPL.3 Curb should not be used synonymously with LP desmitis. Although not directly studied, CSA measurement (see Figure 78-7) of all soft tissue structures should routinely be performed and compared with measurements from the contralateral limb (some horses are bilaterally affected), because common forms of SDF tendonitis and LP desmitis are often associated with increased CSAs rather than frank fiber tearing. Curb is primarily an injury of racehorses, especially STBs. Gait, speed, and training methods differ between racing breeds, and STB racehorses have a higher prevalence of conformational abnormalities, such as sickle-hocked and in-at-the-hock conformation. These conformational abnormalities have not been directly studied, and a causeand-effect relationship is therefore difficult to establish. However, sickle-hocked conformation may increase load on the distal plantar soft tissue structures, predisposing to curb. Weight and load distribution are considerably different in STBs and TBs. Curb develops frequently in STB racehorses that train and race on a thin, near-hard surface, contrary to many soft tissue injuries that result from work on deep surfaces. Many curbs develop in young STB

racehorses early in training when they are jogging and not formally performing speed work. In some instances track surfaces are inconsistent and perhaps slippery, because early training is done in the winter months. In many horses clinical signs are recurrent and progressive, and the development of clinical signs early in training supports a theory that curb develops primarily as a result of overload of plantar soft tissue structures, in a roughly plantar-todorsal direction, because the most common tissue involved is the PT-PL tissues. For instance, in our study SDF tendonitis was not seen in horses without PT-PL tissue enlargement, suggesting that PT-PL injury may have preceded injury of the SDFT.3 Pronounced lameness in horses with SDF tendonitis was seen only when injury progressed distally into zone 2 in the proximal metatarsal region; in some horses sickle-hocked conformation and alleged loss of support of the hock produced what appeared as a dropped hock. Horses with this form of curb, LP desmitis, or combination injury are most likely to be lame. Curb was more common in the LH limb, and although it is tempting to associate this finding with counterclockwise training, many horses developed curb before speed work commenced in that direction. Perhaps in STBs the conventional practice of giving horses many slow miles of jogging in a clockwise direction may place additional load on the outside LH, predisposing to curb. Curb appears more common in pacers than trotters. Nonracehorse sports horses develop curb, but only sporadically, and lameness is often moderate to severe and most commonly is associated with PT-PL tissue swelling, although other structures are sometimes involved.

Peritendonous and Periligamentous Inflammation

PT-PL tissue swelling occurs alone or with abnormalities of one or more of the SDFT, DDFT, or LPL. PT-PL tissue injury can occur secondary to direct trauma from horses kicking a wall or trailer door, or rarely from a direct kick or inter­ ference injury from another horse, resulting in acute, large, painful swelling. Ultrasonographic examination most often reveals frank hemorrhage and edema. More commonly the horse has neither a history of trauma nor clinical findings suggesting trauma. We suspect that PT-PL tissue injury reflects excess loading or strain of the plantar tarsal soft tissue structures from race training. Extensive jogging of young STBs early in training may cause dramatic increase in hock loading, and tension and overstretching of thin PT-PL tissue occurs. PT-PL tissue injury may be an accumulated overload injury and may develop secondarily to other lameness. The PT-PL tissue is most plantar in location, is thin, may be most vulnerable to injury from abnormal strain, and may be the first tissue in progression to be injured. Conformational abnormalities may predispose the horse to such injuries. The cause of such soft tissue injury in mature nonracehorses is unknown, and although swelling can develop with relatively mild lameness, more often lameness is moderate to severe. Clinical examination reveals localized soft tissue swelling, often with heat and pain on palpation, with or without lameness. Previous application of liniments or blisters or pin firing may create sore skin and considerable soft tissue swelling. Ultrasonographic findings depend on the duration of the injury. Acute lesions have an accumulation of anechoic fluid subcutaneously; in more chronic injuries,

Chapter 78  Curb

797

swelling is from subcutaneous echogenic material (see Figures 78-8 to 78-10). The SDFT, DDFT, and LPL should be inspected carefully, but they are frequently normal. Management depends on the degree of lameness, the stage of training, the race or competition schedule, and the owner’s or trainer’s wishes. Blistering is used widely, but we question its value. Although not supported by scientific evidence, thermocautery (pin firing) appears to be an effective management tool, perhaps because it enforces rest. However, prolonged rest is rarely necessary in racehorses, and many horses can be managed by local injection of corticosteroids (triamcinolone acetonide, 9 mg) without substantial interruption of training. More than one treatment may be required if the swelling and lameness do not resolve. A lame horse must be rested to prevent injury to deeper structures. In nonracehorses with moderate-tosevere lameness, lameness may take several weeks to resolve. If the swelling becomes firm, fibrous, and pain free but lameness recurs, further investigation is warranted, because other causes of tarsal pain often develop in STB and TB racehorses with curb. Infection can occur from direct trauma with skin penetration, previous injection, or severe topical counterirritation. If infection is suspected, cytological examination and culture are indicated. If a hematoma resulting from trauma is large or recurrent or if the curb is infected, establishing drainage is often necessary. A distal incision is made to provide drainage, and fibrin and debris are removed. Care must be taken to avoid penetration of the tarsal sheath when creating the incision. A drain is inserted if necessary, and the hock is bandaged. Culture usually reveals Staphylococcus species, and appropriate antimicrobial and NSAID therapy is instituted. Horses are rested for 2 to 3 weeks to allow the tissues to heal, even though lameness from PT-PL tissue injury was not present before infection developed. Prognosis in horses with infection of PT-PL tissues is excellent but is far worse in those with infection of the SDFT, DDFT, or tarsal sheath.

Superficial Digital Flexor Tendonitis

A common finding in horses with curb is SDF tendonitis. Sickle-hocked conformation may predispose the horse to tendonitis, which can occur alone but rarely is seen without concomitant inflammation of the PT-PL tissues. Pathogenesis likely involves progressive or accumulated overload injury of first the thin, fragile PT-PL tissues and later the SDFT. Previous PT-PL tissue injury appears to predispose to subsequent SDF tendonitis if the training level is increased quickly. PT-PL injury may simply be an early stage of a progressive lesion that eventually involves the SDFT or LPL. Progressive injury occurs frequently if horses with PT-PL tissue injury are treated with cryotherapy, internal blisters, or corticosteroids, and training intensity is accelerated before mature fibrous tissue can form. In horses with PT-PL tissue injury and SDF tendonitis, lameness varies, but it is much more likely to be observed than in horses with only PT-PL tissue injury. Lameness may be acute in onset and often is seen at fast speeds, but it can be seen in some horses at a trot in hand. SDF tendonitis occurs commonly in young STB racehorses but usually at a later stage of training than PT-PL tissue injury. Ultrasonographic examination reveals enlargement of the CSA of the SDFT, with a

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PART VIII  The Soft Tissues

variable change in echogenicity and fiber pattern, depending on the severity of the injury (see Figure 78-11). Often, subcutaneous edema or fibrosis occurs, depending on the chronicity of the injury. In horses with SDF tendonitis, rest is an important part of management. Lesions usually are localized to the plantar aspect of the tarsus; those extending farther distally are associated with more severe lameness, and horses have a poorer prognosis. Horses with localized lesions have a fair prognosis, although the prognosis is worse in trotters than in pacers. Horses with mild acute SDF tendonitis, with enlargement of the tendon without fiber tearing, should be rested for 3 to 4 weeks. Without rest, progressive fiber damage may occur, resulting in prolonged recovery. Horses with more severe injuries may require up to 4 months of stall rest and controlled walking exercise. In some STB racehorses actively racing, SDF tendonitis can be managed symptomatically, without giving rest, if the lesion is well localized and mild. Rest is always the best option but one often met with resistance from trainers. Mild lameness may be observed at speed or while the horse is trotting in hand, but severe lameness should not be evident. Ultrasonographic examination often reveals PT-PL tissue injury with enlargement of the SDFT, but core lesions are not present. In most horses local therapy using cold water hosing and poultice application, NSAID therapy, and subcutaneous injection of a corticosteroid preparation is successful. Subcutaneous injection of methylprednisolone acetate (200 mg) and Sarapin (25 mL) medial, plantar, and lateral to the SDFT is often done by practitioners with apparent success. Care is taken not to inject corticosteroids directly into the substance of the SDFT and LPL. Horses are given 10 to 14 days of jogging and light training before racing again. Nonracehorses with localized lesions usually respond well to rest for up to 3 months and have a favorable prognosis. Intralesional injections of fresh bone marrow, platelet-rich plasma, cultured stem cells, or other preparations may help healing and improve long-term prognosis, but we currently have no experience with intralesional therapy in this location. Horses with severe SDF tendonitis have severe mushy swelling. If not given rest, these horses develop progressive tearing of the SDFT distal to the hock in the metatarsal region and lose support of the hock. Long-term rest (9 to 12 months) is recommended, but prognosis for return to previous race class is poor and in trotters, grave.

Deep Digital Flexor Tendonitis

DDF tendonitis is a rare cause of curb. Horses with curb resulting from DDF tendonitis are usually acutely lame and have substantial swelling. Mixed injury with DDF tendonitis accompanying SDF tendonitis and LP desmitis occurs, but it is unusual. Horses with DDF tendonitis have concomitant PT-PL tissue inflammation and effusion of the tarsal sheath (tenosynovitis). The DDFT simply can be enlarged compared with the contralateral limb or can have anechoic or hypoechoic core lesions. During ultrasonographic examination, the DDFT should be evaluated carefully from the midline and plantaromedial aspects. Lameness often is pronounced, and rest is recommended for a minimum of 4 to 6 months, but prognosis is guarded because lameness can recur. Serial ultrasonographic

examination, corrective shoeing, and controlled exercise are given.

Long Plantar Desmitis

LPL injury usually causes acute lameness, but chronic soft tissue swelling and progressive lameness can occur. Soft tissue swelling often is pronounced. Although LP desmitis can occur in racehorses, this form of curb appears to be equally common in other types of horses, such as Western performance horses. In one of the Editor’s experience (SJD) LP desmitis is rare in sports horses in Europe. LP desmitis can be well localized or diffuse. Cross-sectional measurements of the LPL are critical, because desmitis often manifests as ligament enlargement rather than overt fiber tearing. Subtle thickening of the LPL may cause high-speed lameness, and evaluation of the CSA may be the only method to identify early lesions in these horses. Lesions can occur at any level within zones 1A and 1B, and injury may involve the insertion of the LPL on the MtIV (see Figure 78-12). Conservative management is best for horses with LP desmitis, because lameness and swelling often are pronounced. Owners and trainers of nonracehorses are often open to a conservative approach involving ample rest (3 months) to rehabilitate horses with curb properly. Intervening with therapy to enforce rest is not necessary. Controlled return to exercise is straightforward in this type of horse, because walking and trotting under saddle can be given easily. Graded exercise programs are not administered as easily or desired in STB racehorses compared with nonracehorse sports horses. Lunging and walking and trotting under saddle are usually not practical, although riding trotters is popular among trainers originally from Europe. Walking and light jogging in a jog cart are the best methods for graded exercise in a STB racehorse. We do not recommend turnout exercise in any horse with soft tissue injury, because we feel strongly that this prolongs recovery and may lead to reinjury, but we realize our recommendations may not be followed. Cryotherapy, topical counterirritants, subcutaneous injections, and thermocautery are less likely to influence inflammation and healing of the LPL than more superficial causes of curb, but these treatments are sometimes requested. As experience is gained with intra­ lesional therapy for management of soft tissue injuries in horses, it will undoubtedly be applied to injuries in the plantar aspect of the tarsus. Curb can result from LP desmitis at its insertion on the MtIV. These horses do not have extensive swelling but focal thickening just proximal to the MtIV. Mild soft tissue swelling must be differentiated from a prominent but normal MtIV seen in yearlings with sickle-hocked conformation. Horses with curb resulting from distally located LP desmitis show lameness and mild, focal swelling and are managed with rest.

Mixed Soft Tissue Injuries

Ultrasonographic examination of curb nearly always identifies PT-PL tissue inflammation and in many horses an abnormality of the SDFT, DDFT, or the LPL. Occasionally, however, simultaneous injury of the SDFT and LPL occurs in addition to PT-PL tissue inflammation. This is most common in nonracehorse sports horses, in which lameness and swelling are severe. Long-term rest is recommended, but prognosis is guarded.

Chapter 79  Bursae and Other Soft Tissue Swellings



Chapter

79 

Bursae and Other Soft Tissue Swellings Sue J. Dyson

799

NAVICULAR BURSA The navicular bursa is discussed in Chapters 24 and 30.

TROCHANTERIC BURSA The Editors have no clinical experience of trochanteric bursitis. This condition is discussed further in Chapter 47.

CALCANEAL BURSA A bursa is a flattened, closed sac interposed between structures subject to friction or at points of unusual pressure, such as bony prominences and tendons. Bursae are lined with a cellular membrane resembling synovium and are classified according to position (subcutaneous, subligamentous, submuscular, and subtendonous) and according to the method of formation (congenital or acquired). Acquired bursae develop because of pressure and friction over bony prominences. Tearing of the subcutaneous tissues results in accumulation of transudative fluid, which becomes encapsulated by fibrous tissue. In chronic injuries fibrous bands may develop within the capsule.

SUPRASPINOUS BURSA

References on page 1320

The supraspinous bursa overlies the summits of the dorsal spinous process of the second to fifth thoracic vertebrae, under the funicular part of the nuchal ligament. Inflammation of the supraspinous bursa and surrounding soft tissues, so-called fistulous withers, is usually infectious in origin and may be a sequela to trauma. Streptococcus and Staphylococcus species, Brucella abortus, and Onchocerca cervicalis have been considered important causative agents.1-3 Clinical signs of supraspinous bursitis are generalized soft tissue swelling, heat and pain, and often draining tract(s). Osteitis or osteomyelitis of the dorsal spinous processes of the cranial thoracic vertebrae may be concurrent. Care must be taken not to misinterpret the normal granular radiopaque appearance of normal, incompletely ossified summits of the dorsal spinous processes.4 Diag­ nostic ultrasonography and radiology are useful for determining the extent of the infection, for identifying a foreign body, and for evaluating signs of osteitis or osteomyelitis. Treatment is by aggressive surgical debridement of all infected tissue and establishment of adequate drainage, taking care not to penetrate the dorsoscapular ligament. Several surgical procedures may be required to resolve the infection successfully.1-3

The calcaneal or intertendonous bursa lies between the tendons of the gastrocnemius and the superficial digital flexor muscles, proximal to the hock, and extends distally on the plantar aspect of the calcaneus to the distal aspect of the hock (Figure 79-1). In most horses a communication exists between the calcaneal bursa and the gastrocnemius bursa. There is communication between the calcaneal bursa and the subcutaneous bursa in 37% of horses. Injuries of the calcaneal bursa are not common and are usually the result of trauma. However, mild distention of the calcaneal bursa often is seen with gastrocnemius tendonitis (see page 803). Mild distention also may be seen unilaterally or bilaterally, as an incidental finding unassociated with lameness.5 Primary inflammation of the bursa results in acute-onset lameness associated with distention of the bursa. Hemorrhage into the bursa also may occur. Conservative management by rest, with or without injection of short-acting corticosteroids, usually results in resolution of lameness, although enlargement of the bursa may persist. More commonly, infection of the bursa is caused by a penetrating injury or is secondary to infectious osteitis of the calcaneus6,7 (see Chapter 44). Chronic distention of the calcaneal bursa also has been seen with well-circumscribed osteolytic lesions on the

Gastrocnemius bursa Calcanean bursa

Plantaroproximal pouch of tarsocrural joint capsule

Dorsal pouch of tarsocrural joint capsule

INTERTUBERCULAR (BICIPITAL) BURSA The intertubercular (bicipital) bursa is discussed in Chapter 40.

HYGROMA Hygroma is discussed in Chapters 38 and 67.

Fig. 79-1  •  Diagram of a sagittal section of the hock region showing the relative positions of the calcaneal and gastrocnemius bursae.

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PART VIII  The Soft Tissues

tuber calcanei, which were thought to represent enthesopathy at the insertion of the gastrocnemius tendon.8 Further investigation should include diagnostic ultrasonography, radiography of the calcaneus, and synoviocentesis. Radiographic examination should include a flexed skyline image of the calcaneus.9 The internal structure of the bursa may be evaluated endoscopically,10 but some underlying bony lesions may not be visible if the insertion of gastrocnemius is intact.8 Endoscopy has been used diagnostically and therapeutically in horses with infectious osteitis, or bursitis, and in those with osteolytic lesions. Horses with primary infection of the calcaneal bursa should be treated by debridement and lavage of the bursa and broad-spectrum antimicrobial therapy. Horses with infectious and noninfectious lesions of the calcaneus have been managed conservatively and surgically, with rather disappointing results.6-8 Repeated surgeries are often required, and a substantial number of treated horses have persistent lameness.

SUBCUTANEOUS ABSCESS OVER THE TUBER CALCANEI Puncture wounds in the region of the hock frequently result in penetration of the calcaneal bursa and infectious bursitis. Less commonly a subcutaneous abscess develops associated with firm, painful swelling on the plantar aspect of the hock and lameness. The extent of soft tissue swelling may make accurate palpation difficult, and ultrasonography is essential to determine whether or not the calcaneal bursa is involved. Radiographic examination of the calcaneus is also required. Treatment is by radical surgical debridement. The long-term functional outcome is usually satisfactory, although there is usually residual swelling (capped hock).

GASTROCNEMIUS BURSA The subgastrocnemius bursa usually communicates with the calcaneal or intertendonous bursa. Mild distention may be present, unassociated with lameness. Primary injuries of the gastrocnemius bursa are rare. The bursa may be distended in association with gastrocnemius tendonitis, resulting in a capped hock appearance (see page 804). Occasionally, infection may occur because of a puncture wound or extension of infection from the calcaneal bursa.

CAPPED HOCK A capped hock appearance may be caused by distention of the gastrocnemius bursa, distention of the subcutaneous bursa, or development of an acquired bursa over the tuber calcanei (see Figure 6-28). An acquired bursa develops because of repetitive trauma, such as the horse kicking the stable walls or leaning backward on its hindlimbs when traveling. Capped hock usually has no associated lameness. Protection of the hocks with hock boots may help to prevent deterioration.

CUNEAN BURSA The cunean bursa lies underneath the cunean tendon on the medial aspect of the hock. Inadvertently penetrating

the bursa is easy if one is inexperienced in injecting the centrodistal joint. Although the potential for primary bursitis exists, neither of the Editors of this text recognizes primary bursitis as a cause of lameness in racehorses or other sports horses. Gabel recognized a syndrome, “cunean tendonitis and bursitis–distal tarsitis syndrome of harness racehorses,” but appreciated that horses showed substantially better improvement in gait after intraarticular analgesia of the distal hock joints than after infiltration of the cunean bursa alone.11 Nonetheless, a component of periarticular soft tissue pain may occur in Standardbred trotters and pacers with distal hock joint pain, and treatment of the cunean bursa with corticosteroids frequently is used as part of management. Cunean tenectomy is practiced by some, but it has largely fallen from favor. Subcutaneous injection of corticosteroids and Sarapin over the proximal aspect of the second metatarsal bone may yield better results than medication of the cunean bursa.5

CAPPED ELBOW A capped elbow is an acquired bursa that develops over the olecranon of the ulna. The bursa results from repeated trauma from the heel of the shoe on the ipsilateral forelimb when the horse is lying down. The condition generally is not associated with lameness and is merely a cosmetic blemish. The use of a sausage boot around the pastern prevents trauma from the shoe, and usually the swelling diminishes substantially and rapidly in size. Horses with chronic injuries have been treated by injection of corticosteroids, orgotein, or dysprosium-165, with disappointing results, or surgically, with better cosmetic results.12

ACQUIRED BURSA ON THE DORSAL ASPECT OF A HIND FETLOCK Firm swelling on the dorsal aspect of the hind fetlocks of horses that jump fixed fences is common. These lesions are false bursae that overlie the extensor tendon and are usually of no consequence, except cosmetically. However, a puncture wound may result in infection, causing enlargement of the bursa and surrounding soft tissue swelling, localized heat, and pain on palpation.5 In contrast to infection in a joint or tendon sheath, lameness is usually only mild to moderate. Ultrasonography is useful to better identify the causes of the soft tissue swelling, and diagnosis is confirmed by synoviocentesis and identification of many nucleated cells. Surgical treatment is required, and the prognosis is good.

FALSE THOROUGHPIN A thoroughpin is the colloquial name for distention of the tarsal sheath, but more commonly the term is misused to describe a variety of swellings that may develop in the distal aspect of the crus cranial to the gastrocnemius tendon. These conditions are otherwise called false thoroughpins and should be differentiated from distention of the tarsal sheath, tarsocrural joint capsule (see Chapter 44), or calcaneal bursa (see page 799). A false thoroughpin occurs laterally more commonly than medially and may develop unilaterally or bilaterally. A false thoroughpin



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Fig. 79-2  •  Plantar view of a right hock. A false thoroughpin (arrow). The swelling in this horse was acute in onset, but it was unassociated with lameness. The horse was maintained in full work, and despite this the swelling reduced in size. Ultrasonographic evaluation revealed a unilocular fluid-filled cavity.

varies in size from small to large. In contrast to distention of the tarsal sheath or the plantar outpouching of the tarsocrural joint capsule, these swellings cannot be balloted from laterally to medially and do not extend distal to the hock (Figure 79-2). They may be sudden or insidious in onset and may or may not be associated with lameness. The causes vary and are poorly understood. False thoroughpins are usually solitary, fluid-filled sacs (Figure 79-3), unilocular or multilocular, with a wall of variable thickness, with or without large echogenic fibrous bands traversing them (Figure 79-4). They may develop secondary to local hemorrhage or because of herniation of the tarsal sheath or the calcaneal or gastrocnemius bursae.13-15 Diagnostic ultrasonography is useful to identify the nature and extent of the swelling (see Figure 79-4). Unlike the tarsal sheath, no tendon is within the cavity. Positivecontrast radiography can be used to demonstrate whether any communication exists between adjacent structures (see Figure 79-3). A false thoroughpin may be an incidental clinical finding unassociated with lameness. The condition is seen commonly in horses with a base-narrow hindlimb conformation.5 Other causes should be excluded before one concludes that a false thoroughpin is the cause of lameness. Even if the swelling is acute in onset, in the absence of lameness I have maintained horses in work with no deleterious effects. Sometimes such swellings spontaneously reduce in size, but some swelling is likely to persist. Long-term lameness associated with a false thoroughpin has been seen in a number of horses with chronic hindlimb lameness that has not responded to conservative management. Surgical excision of large multiloculated

Fig. 79-3  •  Dorsolateral-plantaromedial oblique radiographic image of a hock. A positive-contrast radiographic study of false thoroughpin. This fluid-filled cavity did not communicate with the tarsal sheath.

Fig. 79-4  •  Longitudinal ultrasonographic image of a false thoroughpin. Proximal is to the left. There is a thick-walled fluid-filled cavity with some echogenic bands.

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PART VIII  The Soft Tissues

cystlike lesions has resolved lameness successfully in some horses,5 although cosmetic results may be disappointing.

Spherical Masses Close to the Fetlock

Small, focal, hard, nonpainful spherical swellings are sometimes seen on the palmarolateral (plantarolateral) or

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palmaromedial (plantaromedial) aspect of the fetlock adjacent to the digital flexor tendon sheath (DFTS). These do not generally cause lameness. Ultrasonographic examination reveals a fluid-filled mass. Lameness associated with herniation of the DFTS is discussed in Chapter 74, page 776.

Chapter

80 

Other Soft Tissue Injuries Sue J. Dyson RUPTURE OF THE FIBULARIS (PERONEUS) TERTIUS Anatomy

The fibularis (peroneus) tertius is an entirely tendonous muscle that lies between the long digital extensor and the cranialis tibialis muscles, which cover the craniolateral aspect of the tibia. The fibularis tertius originates from the extensor fossa of the femur. Distally the fibularis tertius divides into branches that enfold the tendon of insertion of the tibialis cranialis and insert on the dorsoproximal aspect of the third metatarsal bone, the calcaneus, and the third and fourth tarsal bones. The tendon is an important part of the reciprocal apparatus of the hindlimb, which coordinates flexion of the stifle and hock.

The fibularis tertius is the most echogenic structure on the craniolateral aspect of the crus and is identified readily by ultrasonography as a well-demarcated hyperechogenic structure relative to the surrounding muscles (Figure 80-1).

History and Clinical Signs

Rupture of the fibularis tertius invariably is caused by trauma resulting in hyperextension of the limb; for example, a horse trying to jump out of a stable and getting one hindlimb caught on the top of the stable door. This usually results in rupture of the tendon in the middle of the crus but occasionally farther distally. Alternatively, rupture may be caused by a laceration on the dorsal aspect of the tarsus, resulting in transection of the tendon. Occasionally, partial tearing of the tendon occurs, usually at the level of the tarsocrural joint, with prominent swelling. Occasionally the reciprocal apparatus is partially but not totally disrupted. Avulsion injuries of the origin of the tendon rarely occur in young foals. Injury close to the origin is unusual in mature horses, occurring in two of 25 adult horses with fibularis tertius injury.1 The clinical signs are pathognomonic, because rupture of this tendon allows the hock to extend while the stifle is flexed. When standing at rest, the horse may appear

Fig. 80-1  •  Transverse ultrasonographic images of the craniolateral aspect of the midcrus of 7-year-old horse with left hindlimb lameness of 2 months’ duration. The fibularis tertius is the most echogenic structure in the center of the image of the right (R) hindlimb (solid arrow). Compare this with the image of the left (L) hindlimb, in which the fibularis tertius is markedly hypoechoic (open arrow). Note also that the overlying muscle is increased in echogenicity compared with the right hindlimb.

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should be monitored ultrasonographically. Fifteen of 21 horses (71%) retuned to full athletic function, with a mean convalescent period of 41 weeks.1 Performance horses were less likely to return to their former activity than pleasure horses. Site and cause of injury (laceration or trauma) did not influence the outcome, but the presence of other injuries adversely influenced the prognosis. Delayed recognition of the clinical signs and failure to confine the horse may result in a chronic lesion, which fails to heal satisfactorily. However, compensatory hypertrophy and/or fibrosis of surrounding muscles may permit functional recovery.1,2

COMMON CALCANEAL TENDONITIS

Fig. 80-2  •  A horse with rupture of the fibularis tertius. The hock can be extended while the stifle is flexed. Note also the characteristic dimple in the contour of the caudodistal aspect of the crus. Clinical signs developed after the horse had attempted to jump out of its stable and had got hung up on the door. The horse made a complete recovery.

clinically normal, although with acute injury careful palpation may reveal some muscle swelling on the craniolateral aspect of the crus or farther distally. When the horse walks, it should be viewed carefully from behind and from the side. The hock may extend more than usual. The tendons of gastrocnemius and the superficial digital flexor muscles may appear unusually flaccid, and a dimple is seen on the caudal aspect of the crus about one handbreadth proximal to the tuber calcanei. At the trot the horse appears severely lame, with apparent delayed protraction of the limb because of overextension of the hock. If the limb is picked up and pulled backward, the hock can be extended gradually and “clunks” into complete extension while the stifle remains flexed. A characteristic dimple appears in the contour of the caudal distal aspect of the crus (Figure 80-2). If rupture is only partial, or if lameness is chronic and some repair has taken place, clinical signs may be less severe and the diagnosis less obvious. Presumably, strain of this tendon can occur, resulting in lameness, but I have no experience of this, and to my knowledge this condition has not been documented.

Diagnosis

The diagnosis of rupture of the fibularis tertius is based on the pathognomonic clinical signs. The site of rupture can be identified with ultrasonography (see Figure 80-1). The normally echogenic structure is not clearly identifiable and may be replaced by a region that is hypoechoic relative to the surrounding muscles. In horses with chronic injuries the surrounding muscles may become hypertrophied. Usually no associated radiological abnormalities are apparent in adult horses, although avulsion fracture of the origin has been described in foals.

Treatment

Confinement to box rest for 3 months, followed by a slow resumption of work, usually results in total resolution of clinical signs. Most horses are able to return to full athletic function without recurrence of clinical signs; however, injury may recur if work is resumed prematurely. Healing

The common calcaneal tendon consists of components from the superficial digital flexor and gastrocnemius tendons and from the biceps femoris, soleus, semimembranosus, and semitendinosus muscles. Contributions from the last two muscles are called the axial and medial tarsal tendons. So-called “common calcaneal tendonitis” has resulted from a kick in the hock region.3 Unfortunately, the horse was not examined with ultrasonography until 5 months after injury, at which time soft tissue swelling was marked. Ultrasonographic examination revealed that the superficial digital flexor and gastrocnemius tendons appeared normal, but the axial and medial tarsal tendons were enlarged. The horse made a complete functional recovery.

GASTROCNEMIUS TENDONITIS Tendonitis of the gastrocnemius is a relatively unusual cause of hindlimb lameness in the horse.4-6 Disruption of the gastrocnemius in neonatal foals is discussed separately.

Anatomy

The gastrocnemius muscle arises from two heads that terminate in the midcrus in a common tendon. Proximally the tendon lies caudal to the superficial digital flexor tendon (SDFT); farther distally the tendon lies laterally and is ultimately cranial, inserting on the tuber calcanei. The SDFT and gastrocnemius tendons are separated by a bursa, the calcaneal or intertendonous bursa, that extends to the midtarsal region. A small bursa, the subgastrocnemius bursa, also lies cranial to the insertion of the gastrocnemius tendon on the tuber calcanei. A communication usually exists between these bursae. The intertendonous bursa also communicates with a subcutaneous bursa in approximately 37% of horses. The tendon of the gastrocnemius may still contain some muscular tissue as far distally as the level at which it lies lateral to the SDFT. This results in hypoechoic regions within the tendon. Gastrocnemius tendonitis usually occurs distally, distal to the musculotendonous junction. Rarely, damage occurs at the musculotendonous junction.7 Occasionally, injuries occur at the origin of the gastrocnemius on the distal caudal aspect of the femur.8

History and Clinical Signs

Lameness may be acute or gradual in onset and varies from mild to severe. Distention of the subgastrocnemius and

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PART VIII  The Soft Tissues

Fig. 80-4  •  Transverse ultrasonographic image of the caudal distal aspect of the crus of a 6-year-old mare with left hindlimb lameness that was alleviated by perineural analgesia of the tibial nerve. Medial is to the left. The gastrocnemius tendon is enlarged, its caudal lateral aspect is poorly defined (arrowheads), and there is a large hypoechoic region consistent with gastrocnemius tendonitis. Fig. 80-3  •  Medial view of the left hock of a 7-year-old Thoroughbred with acute-onset lameness associated with gastrocnemius tendonitis. Note the capped-hock appearance (black arrowhead) and the distention of the calcaneal bursa (white arrowhead).

calcaneal bursae frequently is associated with gastrocnemius tendonitis, and the horse often develops a cappedhock appearance because of distention of the subcutaneous bursa (Figure 80-3). However, these swellings can occur without lameness or detectable pathological conditions of the gastrocnemius or SDFT (see page 799). Mild enlargement of the gastrocnemius tendon may occur, but this can be difficult to appreciate. Eliciting pain by palpation usually is not possible. Occasionally there are no palpable abnormalities. Severe lameness is characterized by a reduced height of arc of foot flight, shortened cranial phase of the stride, and a tendency to hop off the caudal phase of the stride. Horses with less severe lameness have no specific gait characteristics. Lameness often is accentuated by proximal or distal limb flexion. Two of four horses with injury to the origin of the gastrocnemius muscle had an unusual gait characterized by internal rotation of the affected limb (outward movement of the calcaneus).8 One of the Editors (MWR) has seen a horse with gastrocnemius tendonitis exhibit a similar, unusual gait in the affected limb. Care should be taken to not overinterpret this clinical finding in sound horses, because bilaterally symmetrical internal rotation of the hindlimbs can be a normal finding. A severe injury at the origin of the gastrocnemius muscle may result in an abnormal posture, with the hock of the affected limb lower than that of the contralateral limb.

Diagnosis

Lameness associated with gastrocnemius tendonitis is improved substantially by perineural analgesia of the tibial nerve, possibly because of local diffusion of the local

anesthetic solution. Diagnosis is confirmed by ultrasonographic examination. Comparison with the contralateral limb is useful. Lesions usually occur distal to the musculotendonous junction but do not involve the insertion on the tuber calcanei. The tendon usually is damaged in the distal aspect of the crus, where it lies cranial to the SDFT. Ultrasonographic abnormalities include enlargement of the tendon, poor definition of the margins, and focal or diffuse hypoechoic or anechoic regions (Figure 80-4). Usually no detectable radiological abnormalities are apparent. In young Thoroughbred racehorses there may be increased radiopharmaceutical uptake (IRU) in the tuber calcanei, which should prompt investigation of the gastrocnemius tendon as a potential cause of lameness. Ultrasonographic assessment of the gastrocnemius tendon is also warranted if lameness is abolished by perineural analgesia of the tibial and fibular nerves, but no potential cause of lameness is identified in the hock or proximal metatarsal regions. Injury at the origin of the gastrocnemius muscle on the caudal aspect of the femur may be associated with IRU and, if chronic, radiological evidence of proliferative new bone formation.8

Treatment and Prognosis

Conservative treatment with box rest and controlled exercise for up to 12 months generally has resulted in progressive improvement in lameness associated with gastrocne­ mius tendonitis and improvement in the ultrasonographic appearance of the tendon. Horses with mild lesions have been able to return to full athletic function without recurrent lameness, but those with more severe lesions have a more guarded prognosis.5,6 Overall 14 of 25 horses managed conservatively have returned to full athletic function.9 However two horses with moderate or severe lesions that

failed to respond to conservative management subsequently returned to full athletic function after intralesional treatment with β-aminopropionitrile fumarate.9 Three of four horses with injury of the origin of the gastrocnemius returned to athletic use, but recurrent injury occurred in the fourth horse.8

DISRUPTION OF THE GASTROCNEMIUS IN NEONATAL FOALS Disruption of gastrocnemius in neonatal foals is an unusual cause of hindlimb lameness or an inability to stand.10,11 The condition has often been associated with dystocia. Partial or complete rupture usually occurs at the proximal musculotendonous junction, resulting in soft tissue swelling over the caudodistal aspect of the femur. Injury is usually unilateral, although it is occasionally bilateral. Diagnosis is based on the stance of the foal and detection of soft tissue swelling and is confirmed by ultrasonography. Foals able to bear weight are treated by stall rest alone; a sleeve cast or splints are applied to those that are unable to load the limb. Complications include severe hemorrhage associated with the injury, leading to cardiovascular compromise (three of 28 foals, 11%); concurrent disease (17 of 28, 61%); abscess formation at the site of rupture (four of 28, 14%); and cast sores (seven of 18, 39%).11 Historically the prognosis was considered guarded,10 but in a recent report 23 (82%) of 28 foals survived to discharge from the hospital, and 13 (81%) of 16 horses that reached 2 years of age trained or raced.11

SUBLUXATION AND LUXATION OF THE SUPERFICIAL DIGITAL FLEXOR TENDON FROM THE TUBER CALCANEI Lateral (see Figure 6-29), or less commonly medial, luxation or subluxation of the SDFT from the point of the hock may occur along with damage to or rupture of the retinacular bands that insert medially and laterally on the tuber calcanei. Although usually a unilateral injury, the condition can occur bilaterally. Lateral displacement of the SDFT occasionally occurs secondarily to hyperextension of the hind fetlock associated with progressive breakdown of the suspensory apparatus in older horses (see Figure 72-24 and page 760).

Anatomy

The SDFT lies caudally in the distal aspect of the crus and broadens to form a cap over the tuber calcanei. At this level, broad, thick retinacular bands extend medially and laterally to insert on the tuber calcanei. The calcaneal bursa is interposed between the SDFT and the tendon of gastrocnemius.

History and Clinical Signs

Partial or complete disruption of one of the retinacular bands that attach the SDFT to the tuber calcanei can result in subluxation or, more commonly, luxation of the SDFT laterally or medially. Occasionally the SDFT tendon splits sagittally, with the tendon luxating both medially and laterally. Lameness is usually sudden in onset and severe, although occasionally mild lameness precedes this, associated with soft tissue swelling in the region of the

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point of the hock. Frequently no history of trauma is apparent, and the injury often occurs as the horse is being worked. The horse may suddenly stop and may become extremely distressed, especially if the tendon repeatedly moves on and off the tuber calcanei. The horse may kick out repeatedly with the limb. The tendon may return to its normal position when the horse bears weight. Soft tissue swelling rapidly ensues, resulting in a capped hock appearance, making accurate palpation difficult. If the horse is kicking repeatedly when moving, one may conclude wrongly that the soft tissue swelling developed as the result of trauma caused by kicking. With subluxation of the SDFT, the tendon is usually positioned normally at rest. Careful observation of the tendon as the horse moves may reveal instability. With luxation it may be possible to see that the SDFT has been displaced laterally or, less commonly, medially. If the tendon remains luxated, then the horse tends to be less agitated, although obviously in pain in the acute stage. Careful palpation may reveal instability of the tendon or its displacement to an abnormal position. In horses in which lateral displacement occurs secondary to hyperextension of the fetlock, the condition may be insidious in onset and slowly progressive and unassociated with acute lameness.

Diagnosis

Ultrasonographic examination is helpful if the tendon is displaced by confirming its abnormal position, but such examination can add to confusion if the tendon is in the normal position when the horse stands still. It may be possible to identify a partial tear in the medial, or less commonly the lateral, retinacular band. The calcaneal bursa may be distended, and if the condition is chronic there may be synovial proliferation. Occasionally there is a longitudinal split in the SDFT, which adversely affects prognosis.

Treatment

In the acute stage pain relief is essential, and tranquilization may be necessary to calm the horse. If the SDFT is unstable and is moving constantly on and off the tuber calcanei, management in the acute and chronic phases may be difficult. If the tendon is permanently dislocated laterally or medially, the distress usually resolves rapidly. Antiinflammatory drugs are best avoided, because the surrounding soft tissue swelling helps stabilize the tendon. If the tendon has luxated laterally, prolonged rest (6 months) usually results in resolution of pain, although a mechanical lameness may persist. This limits the horse’s function for dressage, but these horses may be able to race or show jump at a high level. The prognosis associated with medial luxation is more guarded and tends to be associated with a greater degree of mechanical lameness. If the SDFT is unstable initially, the tendon may with time and progressive further disruption of the attaching retinacular bands become more stable in a luxated position. Peritendonous injection of a sclerosing agent, P2G (Martindale Pharmaceuticals, Romford, Essex, England), has been helpful in stabilizing the luxated tendon in a limited number of horses.9 Surgical transection of a partially torn retinacular band has helped in chronic subluxation.9 Attempts at surgical stabilization of the SDFT in its normal position often have been disappointing, although

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PART VIII  The Soft Tissues

successful results have been reported.12,13 Surgical stabilization is worth considering only if the horse is temperamentally suited to a full-limb cast. Prognosis is influenced by the ease of reconstruction of the torn retinaculum, which depends on the site of the tear (close to the tendon, close to the bone, or midway) and its age.

BICEPS BRACHII TENDONITIS Biceps brachii tendonitis is discussed in Chapter 40.

INFECTION OF THE COMMON DIGITAL EXTENSOR TENDON Infection of the common digital extensor tendon and its sheath is usually the result of a puncture wound with or without deposition of a foreign body such as a blackthorn. It results in swelling, heat, pain, and lameness (see also page 789). Successful management was described by complete resection of the infected tendon.14

Chapter

81 

wire or a sharp object over which the horse has jumped. The flexor (palmar or plantar) aspect of the limb may be traumatized by circumferential wire injuries, landing on a sharp object, or being struck. The latter may be self-inflicted or from another horse.

Tendon Lacerations Sue J. Dyson and Alicia L. Bertone

References on page 1321

Tendon lacerations are serious injuries in horses because of the loss of the biomechanical function of the tendon, the slow return of tendon strength, the immediate strenuous loading demanded by a horse, and the complications of scarring. Nonetheless, early diagnosis, wound management, limb support, and long-term surgical and medical management have resulted in a good prognosis for most horses with extensor tendon lacerations and a fair prognosis for most of those with flexor tendon lacerations.1,2 The extensor (dorsal) aspect of the limb is often damaged by

DIAGNOSIS Gross Appearance of the Wound

Any laceration over the dorsal or palmar/plantar surface of the limb distal to the stifle or elbow, especially across the dorsal aspect of the tarsus, distal dorsal aspect of the tarsus, dorsal metatarsal region, distal aspect of the radius, dorsal metacarpal region, and dorsal fetlock region may involve a tendon (Figure 81-1). Extensor tendons and the superficial digital flexor tendon (SDFT) are positioned directly under the skin; therefore minor-appearing wounds can transect these tendons completely. Direct visual inspection may reveal transected tendon fibers protruding from the

ECRM CDE

Lateral digital extensor muscle

DDFM

LDE

Long digital extensor muscle

SDFM

3 3

Tibialis cranialis muscle

4

A Lateral

2

SL

5 C

B Medial

1

2

6

4

1

D Lateral

Medial

Fig. 81-1  •  Diagram illustrating common sites of tendon injury. A, Lateral forelimb. B, Medial forelimb. C, Lateral hindlimb. D, Medial hindlimb. 1, Dorsal tarsus; 2, dorsal metatarsal region; 3, distal radius; 4, dorsal metacarpal region; 5, dorsal fetlock region; 6, palmar metacarpal region; ECRM, extensor carpi radialis muscle; CDE, common digital extensor muscle; LDE, lateral digital extensor muscle; DDFM, deep digital flexor muscle; SDFM, superficial digital flexor muscle; SL, suspensory ligament. (Adapted from Bertone AL: Tendon laceration in tendon and ligament injuries. Part II, Vet Clin North Am Equine Pract 11:293, 1995.)



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wound. However, injuries sustained at the gallop may result in a skin wound removed from the site of tendon damage because of the movement of the skin during exercise. The position of the wound relative to synovial structures should be evaluated with care because concurrent synovial contamination or infection reduces the prognosis and necessitates specific emergency treatment.

Evaluation of Gait

Each tendon serves a biomechanical function. Complete severance of a tendon results in a posture or gait change, which may be pathognomonic for disruption of the tendon integrity.

Extensor Tendons

Transection of an extensor tendon below the carpus produces a reduced ability to extend the digit, which is detected as an exaggerated, rapid (uncontrolled) dorsal flip of the hoof at the walk. This subtle change is easiest to detect if the lateral and common (or long) digital extensor tendons are transected completely. Intermittently the horse knuckles at the fetlock joint and places the digit on the dorsal surface of the pastern and fetlock joint. The gait abnormality is more obvious in a hindlimb and with lacerations in close proximity to the fetlock. Remaining peritendonous fascial attachments provide some support in horses with more proximal injuries. Horses with extensor tendon lacerations bear weight fully in a normal posture, unless other aspects of the wound create lameness and pain. Transection of extensor tendons proximal to the carpus and at, or just proximal to, the tarsus also commonly occurs. Proximal to the carpus, transection of the extensor carpi radialis and common digital extensor tendons is most frequent. Flexion of the carpus may cause pain. The tendon sheath is often involved. Proximal or dorsal to the tarsus, transection of the long digital extensor, cranialis tibialis, and fibularis (peroneus) tertius tendons is most frequent. If the fibularis tertius is disrupted, the hock can be extended while the stifle is flexed, indicating loss of the reciprocal apparatus. The gastrocnemius tendon develops a characteristic wrinkle in this extended position (see Figure 80-2 and page 802). The degree of gait abnormality may be mild. Transection of all the extensor tendons over the tarsus still allows full weight bearing with the foot flat on the ground. A greater tarsal extension during the swing phase of the stride and intermittent knuckling of the digit can be detected.

Digital Flexor Tendons

Transection of the digital flexor tendons below the carpus or tarsus produces pain on weight bearing and therefore lameness and gait abnormality. Transection of the SDFT is most common because it has the most superficial position of the two digital flexor tendons. The suspensory ligament (SL) is deep to the deep digital flexor tendon (DDFT) and is therefore least commonly injured with lacerations. A horse with complete transection of the SDFT may stand normally, or it may bear weight on the toe of the hoof to minimize movement of the tendon ends with fetlock joint extension. Complete transection of one branch of the SDFT in the pastern may not alter the stance during full load bearing. Administration of phenylbutazone for pain may eliminate lameness, and a gait abnormality may become

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hard to detect. The DDFT and SL support the fetlock joint together with the SDFT. Therefore slight hyperextension of the fetlock because of disruption of the SDFT may be difficult to detect unless the contralateral limb is picked up. The greater the number of structures transected, the less support to the fetlock and other distal joints and the greater the likelihood of vessel and nerve transection. Elevation of the toe is pathognomonic for transection of the DDFT.

Digital Palpation of the Wound

Digital palpation is a simple and direct way to determine the extent of damage to structures below the skin. Integrity of the tendons is readily determined by feel. Partial tears can be distinguished from complete tears, and this affects treatment (see Partial Tendon Lacerations section). The tendon ends are often palpable beneath the skin proximal and distal to the wound, but they may be removed from the wound if the injury was sustained while the horse was galloping. The muscular attachment to the proximal end pulls the proximal tendon end farther from the wound. The wound should be clipped around the edges and cleansed thoroughly with a dilute antiseptic solution such as chlorhexidine before exploration. Gross debris can be debrided manually from the wound. Sterile gloves should be worn for the digital exploration after the wound is clean. Digital palpation may reveal involvement of a tendon sheath or joint capsule; however, small tears of these synovial structures may not be palpable. Sterile preparation of the skin and injection of a balanced electrolyte solution into the synovial structure in question at a site distant from the wound may demonstrate communication if solution exits the wound. Synovial fluid also can be obtained and submitted for cytological evaluation. Hemorrhage or inflammation is usually present in the synovial fluid if a sheath has been penetrated. Mild inflammatory changes can be seen in synovial structures adjacent to tendon injuries, even if no actual communication with the wound occurs.

Ultrasonographic Evaluation

Ultrasonographic evaluation of the tendons can quantitate the degree of tendon damage, particularly in horses with partial tears. Ultrasonographic examination is not necessary for diagnosing complete tears and therefore is performed rarely. Ultrasonography may also be technically difficult in the region of a skin wound because air in the wound impairs transmission of ultrasound waves. A partial laceration of the SDFT may be associated with the development of longitudinal splits extending proximodistally as a result of altered shear stresses. Complete transection of a branch of the SDFT in the pastern region may result in a shift of position of the branch proximal to the transection toward the side of the intact branch. Ultrasonographic evaluation can be useful during the healing phases of horses with partial or complete tendon lacerations.3 The amount of repair tissue should increase early in repair and then decrease as the tissue matures and gains strength. In digital flexor tendons, about 6 weeks are required for the tendon to gain the strength to support 450 kg, and the strength of the repair tissue is largely because of an increase in tissue mass. The repair tissue cross-sectional area is greater than the original tendon area,

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but the strength of that tissue per unit area is reduced.4 The quality of the repair tissue can be monitored with ultrasonography. Ultrasonographic examinations should show progressively increased homogeneity of echogenicity, reduction in the hypoechoic areas of damaged tendon or early immature repair tissue, and appearance of parallel arrangements of fibers.

EMERGENCY MANAGEMENT Treatment of Shock

Trauma is often severe in horses with lacerated tendons, particularly digital flexor tendons. Some horses may be trapped for hours in wire or entangled in equipment. Blood loss may be extensive if major arteries to the distal limbs have been transected. The loss of the function of a limb is painful and stressful. Initial management of these horses can be lifesaving. If possible, the horse should be caught and brought into a warm, clean area for examination and further treatment. If the horse has severe tachycardia (>100 beats/min) with pale mucous membranes and is reluctant to move, initial treatment should be performed on site. If the wound is still bleeding, a clean pressure bandage should be applied to stop the bleeding and provide some support to the limb. If the function of the limb is impaired mechanically, a splint should be applied over the bandage to minimize further damage with movement. Use of tranquilizers and sedatives should be kept to a minimum until the degree of blood loss and shock can be assessed and treated. Most sedatives are peripheral vasodilators and may produce substantial hypotension in a hypovolemic horse. Some horses may be in stress-induced shock from pain, with extreme catecholamine release. The effect of tranquilizers may be unpredictable and potentially can worsen the bleeding. Securing the horse in a familiar, warm, clean environment and stabilizing the injured limb may resolve the stress-related shock and allow assessment of hemorrhagic shock by evaluating peripheral pulse strength and quality, heart rate, and mucous membrane color. If hemorrhagic shock is severe, the most important treatment is intravenous fluid volume replacement, which can be in the form of high-volume isotonic fluids (20 to 60 L minimum per 450 kg of horse) or hypertonic saline (9% NaCl; 1 L per 450 kg of horse), followed by isotonic fluid replacement. Hypertonic fluid therapy can be effective for rapid expansion of the vascular space in hemorrhagic shock, but hypertonic solutions dehydrate the interstitium and induce a profound renal diuresis. Therefore it is critical that isotonic fluid therapy begins within 30 minutes to 1 hour after hypertonic fluid administration. Hypertonic fluid therapy is practical because of the convenience of the small volumes necessary and works well if the horse is referred or transported to a facility that has access for fluid administration.

Transportation

For transportation the injured limb should be placed toward the back of a trailer. The horse’s weight shifts to the front of a trailer during braking, which is often less controlled than acceleration. The horse’s head should not be tied tightly, so the head and neck can be used for balance. The limb should be supported with a padded pressure bandage and a splint for transport.

MEDICAL MANAGEMENT All horses with tendon lacerations need medical therapy, whether surgery to reappose tendon ends is elected or not. If tendon laceration, partial or complete, is diagnosed, a more thorough aseptic preparation of the wound should be performed. These procedures require sedation, restraint, and local or regional analgesia.

Wound Cleansing and Debridement

The hair should be clipped circumferentially from above the wound (to the estimated top of the bandage) and the entire limb distal to the wound. Drainage of serum and exudate from the wound is often voluminous, and removal of the hair makes subsequent cleaning of the limb easier and more thorough, thereby minimizing bacterial growth and contamination. A 10-minute scrub of the wound with an antiseptic solution should be performed. If bone and tendon are exposed, care must be taken to minimize trauma to these tissues. A minor sterile instrument pack may be helpful in trimming heavily contaminated tissues and lacerated tendon ends, as well as for removing hair and debris from deep in the wound. Lacerated tendons should be trimmed at the edges to remove traumatized tissue that is expected to become necrotic. Debridement of tendon ends should be most conservative in horses with digital flexor tendon lacerations, for which apposition of tendon ends with suture is recommended.

Systemic and Local Medications

Tetanus toxoid should be administered to any horse with a tendon laceration, and tetanus antitoxin should be given if no vaccination history exists. Because all wounds are contaminated at injury and compound wounds have extensive soft tissue injury, broad-spectrum antimicrobial drugs should be administered systemically for a minimum of 3 days. Metronidazole should be considered in horses with grossly contaminated distal extremity wounds. The duration of antimicrobial therapy may be longer in horses with heavily contaminated wounds, wounds healing by second intention, infected wounds, wounds involving a tendon sheath, or wounds with delayed treatment (>24 hours). Wound lavage should be copious, usually with a minimum of 5 L of a balanced electrolyte solution.

SURGICAL TREATMENT Surgery in the form of wound closure is performed in most horses with open wounds involving tendons. Primary closure is preferred, if possible, to provide the best success of obtaining primary wound healing, minimal scar formation, and the fewest complications associated with the transected tendon. However, wounds that are heavily contaminated, older than 24 hours, or heavily traumatized should have a delayed closure (1- to 3-day delay) performed to reduce the contamination and necrotic debris before closure. The decision to close a wound older than 24 hours must be made based on the condition of the wound and surrounding structures. Wounds in horses that have been managed appropriately from the time of injury until surgery can be closed at any time, if tissue loss is minimal and infection is not present.



Extensor Tendons

Transected extensor tendons heal well without primary suturing of the tendon, even if a large gap has formed between the tendon ends. Serial ultrasonographic evaluations show fibrosis occurring between the tendon ends that eventually becomes more organized and regains the linear arrangement of collagen along the pattern of the original tendon. This fibrous tissue seems to provide a mechanical link between the tendon ends because extensor function of the digit returns in most horses. In our experience, a palpable thinning of the new tendon and an enlargement at the old tendon ends usually remains, even after 1 year. Horses with lacerated extensor tendons have a good prognosis, with 73% of injured horses returning to athletic soundness and 18% to pasture soundness.2 In that study, 62% of the affected horses were treated with a three-layer cotton bandage, 23% with a splint and bandage, and 10% with fiberglass casts. It is important that the horse is confined to box rest for at least 6 weeks so that lameness does not ensue. With lameness the hoof may be positioned on the toe, and the force of the digital flexor tendons maintains this position, particularly without the counterforce of the extensor tendon. Chronic flexor pull may result in permanent flexural deformity and lameness. If flexor dominance is noted, a splint or cast should be applied (see Chapter 86). In our experience, the best cosmetic outcome, as well as chances of achieving primary wound closure, occurs with using a fiberglass cast for 3 to 6 weeks. The cast provides the most immobility to the limb and the lacerated tendon ends. Early fibrosis matures more quickly, without disruption of the early granulation tissue.

Digital Flexor Tendons

Horses with complete laceration of one or more digital flexor tendons are best treated with tendon suturing, wound closure, and postoperative immobilization for about 6 weeks. Digital flexor tendons support the weight of the horse on loading. Thus healing and return to full strength is a slow process, one that does not return to normal for at least 6 months. In studies investigating methods of tendon repair, immobilization of the limb in a cast without suturing produced a significantly weaker repair that resulted in the clinical sequela of a hyperextended fetlock joint.4,5 The amount of scar tissue filling the tendon gap was significantly less in this group compared with the sutured groups and was the reason for the reduced strength. Therefore suturing of digital flexor tendon injuries is recommended. Monofilament suture (nylon or polyglyconate) produced the greatest strength of repair compared with carbon fiber suture when placed in a double-locking loop pattern (nylon) or three-loop pulley pattern (polyglyconate) for apposition of tendon ends or for spanning tendon gaps.4-6 The limb should be cast for at least 6 weeks, with the fetlock joint in mild flexion, by building a heel support with casting tape or plaster to provide a level weightbearing surface with the ground. Repairs of flexor tendon lacerations above the hock (i.e., gastrocnemius tendon, DDFT, or SDFT) should follow the same principles, but the prognosis is decreased because of the greater difficulty in maintaining a full-limb cast, larger size of the tendons at this location, and greater biomechanical stresses to support the hock with weight bearing.

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809

Partial Tendon Lacerations

Horses with partially transected tendons can be treated successfully without suturing but with wound closure and limb immobilization. Partial transection of digital flexor tendons usually involves the SDFT only or the axial margin (medial or lateral) of the SDFT and DDFT. If the limb is immobilized, the remaining fibers of tendon provide the stability for the torn tendon ends to remain in apposition and provide the strength to prevent further tendon tearing during healing. Anecdotally, if more than 75% of the SDFT is lacerated, tendon suturing may provide a reduced gap and faster healing and improve the repair. If the SDFT is completely transected along with a partial laceration of the DDFT, the SDFT should be treated with suturing as previously described and the DDFT left unsutured.

Lacerations in Tendon Sheaths

If a laceration enters a tendon sheath, then therapy is altered to include aggressive lavage of the sheath and wound, intrathecal administration of antibiotics, close monitoring of sheath fluid cytological condition, longer use of systemic antibiotics, and limb immobilization. If tissue loss is minimal, wounds entering tendon sheaths should be closed primarily. Primary closure and fiberglass cast application offer the best chance of early healing and minimize the potential for the complications of ascending infection, chronic drainage and fistulae formation, and fibrosis.

CONVALESCENT THERAPY Shoeing

After removal of a cast or splint for horses with extensor tendon lacerations, a gradual return to full weight bearing is recommended. Shoeing recommendations are simple and include trimming or shoeing level, without toe extensions that may catch and produce knuckling. For horses with digital flexor tendon lacerations, an elevated and extended heel shoe can be applied and the heel lowered sequentially over the next 6 weeks to a flat position. For severe lacerations involving the DDFT, SDFT, or SL, an extended heel shoe may always be required for additional flexor support.7

Graduated Exercise

Horses with extensor tendon injuries have not been evaluated as closely during the healing process to assess tissue maturation and return of strength as those with digital flexor tendon injuries. Because the function of the extensor tendon is to extend the digit and not endure a load on weight bearing, return to full strength may occur sooner than for digital flexor tendons. Horses should remain in a box stall or a confined area during the wound healing phases and early fibroblastic repair phases of tendon healing (3 to 6 weeks). After this time, handwalking and controlled exercise such as swimming can begin to strengthen the tendon and improve gliding function. After 10 to 12 weeks of controlled exercise, and if no signs of knuckling or flexor dominance are present, gradual return to athletic use can begin. Horses with digital flexor tendon lacerations require a more gradual convalescent period. After the first 6 weeks of immobilization, the next 6 weeks should be spent in

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PART VIII  The Soft Tissues

confinement and regaining a normal foot posture and full weight bearing. Heel support shoes are applied during this time. After 12 weeks, handwalking can begin and gradually increase in frequency and duration over the next 3 to 6 weeks. Controlled exercise with walking, lunging, swimming, or ponying (leading from another horse) is preferred to turnout. Turnout can be given after the horse is sound at the walk and trot and ultrasonographic examination demonstrates extensive fibrosis and mature scar tissue. Heavy athletic use should not begin until 8 to 12 months after the injury.

PROGNOSIS Successful outcome (soundness) occurs in about 75% of horses with extensor tendon lacerations and up to 54% of horses with digital flexor tendon lacerations.1,2,8 The

prognosis for horses with partial disruption of the SDFT, DDFT, or both is better than for those with complete lacerations.8 Long-term failures are attributable to continued pain from extensive adhesions, joint pain, other injury at the time of laceration, tendon sheath adhesions, tendon contracture, palmar (plantar) annular ligament constriction, reinjury, and failure of the repair to regain adequate strength to support the joint, leading to breakdown. Reinjury to a damaged tendon may occur during healing, but such a tendon can heal successfully, although convalescence is prolonged. In general the prognosis is better for pleasure riding horses than for sports horses, but especially with injuries involving the digital flexor tendons of a hindlimb, complete function may be restored. An association exists between lacerations of either or both the long and lateral digital extensor tendons in the proximal part of the metatarsal region and the subsequent development of stringhalt several months later.9

Chapter

82 

Soft Tissue Injuries of   the Pastern Virginia B. Reef and Ronald L. Genovese

References on page 1321

Injuries to the digital flexor tendons and ligaments in the pastern are a common cause of lameness in horses.1-6 Injuries to the collateral ligaments or the palmar or plantar ligaments of the proximal interphalangeal joint are a less frequent cause of lameness.1,7-9 Swelling, heat, and sensitivity of the affected tendon or ligament to palpation often accompany lameness. Ultrasonographic evaluation of the pastern is indicated when local swelling, heat, and sensitivity are detected, or when effusion occurs in the digital flexor tendon sheath (DFTS).10 The cause of the swelling can be determined by ultrasonography, and the severity of the injury can be characterized. The clinician should keep in mind that peripheral longitudinal splits in the digital flexor tendons within the DFTS are difficult to detect and can be missed ultrasonographically.10 If injury occurs to the superficial or deep digital flexor tendons (SDFT, DDFT) in the metacarpal or metatarsal region, ultrasonographic examination should include an evaluation of these structures in the pastern. Lameness associated with soft tissue injuries of the pastern also can occur without localized soft tissue swelling, and ultrasonographic examination is indicated if pain is localized to the region using diagnostic analgesia and no radiological abnormality is detected, or entheseous new bone is seen. The clinician should bear in mind that intraarticular analgesia of the metacarpophalangeal or metatarsophalangeal joints, the proximal interphalangeal joint, and the DFTS is not necessarily specific and may influence closely related structures such as the distal sesamoidean ligaments and the palmar ligaments of the proximal interphalangeal joint. It also may be important

to use diagnostic analgesia to determine whether the injury causing soft tissue swelling in the pastern region is the source of the lameness. Nuclear scintigraphy may help to determine whether entheseous new bone is active, and magnetic resonance imaging (MRI) has the potential to provide additional information. This chapter focuses on lesions diagnosed using ultrasonography, but the absence of detectable ultrasonographic abnormalities does not preclude soft tissue pathology causing pain.

ANATOMY Most of the soft tissue structures in the pastern are on the palmar or plantar aspects and are similar in the forelimbs and hindlimbs. The following describes the forelimb but applies equally to the hindlimb. The SDFT forms a thin ring around the DDFT at the ergot and in the proximalmost portion of the pastern and then bifurcates into medial and lateral branches. The origin of the branches has a teardrop shape. The cross-sectional area (CSA) of each SDFT branch gradually enlarges as the branch extends distally along the palmarolateral and palmaromedial aspects of the pastern, until the branches insert on the distal aspect of the proximal phalanx and on the proximal aspect of the middle phalanx. The DDFT lies immediately dorsal to the SDFT and extends along the midline to its insertion on the distal phalanx.1-6,11-15 The DDFT has a bilobed shape in the pastern and is surrounded by the DFTS. The oblique (middle) sesamoidean ligaments (OSLs) originate from the base of the lateral and medial proximal sesamoid bones (PSBs) as two large, round to oval branches. These branches become smaller in CSA as they extend distally. The branches join in the proximal to mid aspect of the proximal phalanx and insert as a broad band on the palmar aspect of the middle of the proximal phalanx. The straight sesamoidean ligament (SSL) also has its origin at the base of the PSBs and the palmar ligament and extends distally in the midline, palmar to the OSL, to insert on the scutum medium of the middle phalanx.1-6,11-13,16 The SSL lies dorsal to the DDFT and has an hourglass shape, larger proximally and distally, and narrowest in the middle.



Chapter 82  Soft Tissue Injuries of the Pastern

The DFTS surrounds the SDFT and DDFT throughout the proximal aspect of the proximal phalanx to the bifurcation of the SDFT.1-6,11-15,17 The entire length of the DDFT is included in the DFTS, except for a small area in the distal palmar aspect of the pastern, just proximal to the bulbs of the heel. The dorsal aspect of the DFTS extends farther distally than its palmar aspect. The proximal digital annular ligament is adhered closely to the palmar aspect of the SDFT in the proximal aspect of the pastern.1,3-5,18 The distal digital annular ligament forms a sling over the distal part of the DDFT. These two structures are thin in normal horses. The abaxial and axial palmar ligaments of the proximal interphalangeal joint originate in pairs from the medial and lateral aspects, respectively, of the middle of the proximal phalanx and dorsal to the SDFT branches. They insert on the scutum medium abaxial to the branches of the SDFT (abaxial palmar/plantar ligament) and between the SSL and the branches of the SDFT (axial palmar/plantar ligament). These are large, round to oval ligaments that extend in a diagonal direction from the origin to the insertion. The collateral ligaments of the proximal interphalangeal joint originate from a small eminence on the lateral and medial aspects of the proximal phalanx, distal to the origin of the palmar ligaments, and arc across the joint to insert on a small eminence on the lateral and medial aspects, respectively, of the proximal aspect of the middle phalanx.1,3,7,11 The proximal interphalangeal joint has a closely adhered joint capsule. The common digital extensor tendon is located on the dorsal aspect of the pastern.1 The extensor branches of the suspensory ligament (SL) join the common digital extensor tendon in the distal part of the proximal phalanx. The main insertion of the common digital extensor tendon is on the extensor process of the distal phalanx, but there are also areas of insertion onto the proximal and middle phalanges. A bursa is present between the tendon and the proximal interphalangeal joint.

ULTRASONOGRAPHIC ANATOMY The pastern has been divided into five zones: three zones for the proximal phalanx and two zones for the shorter middle phalanx1-6,12-15 (see Chapter 16).

Superficial Digital Flexor Tendon

In the proximal aspect of the pastern (zone P1A), the SDFT is imaged from the palmar aspect and is homogeneously echogenic and has a thin, half-moon shape in the transverse plane.1-6,12-14 In longitudinal images the SDFT has a parallel fiber pattern and a triangular shape along the midline in zone P1A because its thickness decreases distally. In normal horses, distinguishing the proximal digital annular ligament from the DFTS and the palmar border of the SDFT is difficult. The proximal digital annular ligament can be identified if thickened by following it medially and laterally to its attachment to the proximal aspect of the proximal phalanx. The body of the SDFT ranges in thickness (palmar to dorsal) from 2 to 6 mm in P1A to 1 to 4 mm over the middle of the proximal phalanx.3 The teardrop-shaped branches in the proximal to mid pastern region (at the junction of zones P1A and P1B) are imaged from the palmaromedial and palmarolateral aspects and

811

are followed individually to triangular-shaped insertions. The SDFT branches are similarly homogeneously echogenic, with a parallel fiber pattern throughout. The branches of the SDFT range in thickness from 4 to 7 mm in the proximal pastern to 7 to 12 mm distally.15 The CSA of the two SDFT branches ranges from 0.3 to 0.4 cm2 in the distal portion of zone P1A where the branch begins, increases to 0.4 to 0.6 cm2 in zone P1B, and further enlarges to 0.6 to 0.8 cm2 near the insertion.

Deep Digital Flexor Tendon

The DDFT has an oval to bilobed appearance in the pastern and is imaged on the palmar midline of the pastern until the DDFT is lost from view distally.1-6,12-15 The two lobes are symmetrical. The fibers of the DDFT extend obliquely from a deeper to a more superficial position in the more distal portion of the pastern and are separated from the SSL by an anechogenic space. The dorsopalmar thickness and lateral to medial width of the DDFT decrease in the mid pastern and increase again in the distal aspect of the pastern. The DDFT measures 5 to 10 mm (palmar to dorsal) in the proximal aspect of the pastern, slightly less in the mid pastern, and 7 to 12 mm in the distal aspect of the pastern. The width of the DDFT in a lateral-to-medial direction ranges from 18 to 33 mm in the proximal aspect of the pastern, decreasing to 15 to 23 mm in the mid pastern, and increasing in the distal aspect of the pastern to 23 to 32 mm.3 Along the dorsal aspect of the DDFT in the mid pastern region is a synovial fold of the DFTS that is imaged readily, surrounded by a small amount of anechogenic synovial fluid. In the distal pastern region, the palmar aspect of the DDFT adheres to the synovial membrane of the DFTS.

Oblique Sesamoidean Ligaments

Injury to the OSLs is often missed ultrasonographically because the origin and proximal to midportion of each OSL (where the majority of the injuries are) are not imaged from the palmaromedial and palmarolateral aspects of the limb. The origin of the medial or lateral OSL is best found by placing the ultrasound transducer over the base of the medial or lateral PSB and scanning distally over the bone to its base, angling the transducer proximally to image the origin of the respective OSL.1-6,12,13 Alternatively, the origin of an OSL can be found by following the SL branches distally over the respective PSBs to the base. Immediately distal to the base of the PSB is the origin of an OSL, best located initially in its transverse section as a large, round to oval structure. The OSLs merge in the distal part of zone P1A into a broad, rectangular band dorsal to the DDFT. The OSLs then insert on the palmar or plantar aspect of the proximal phalanx in zone P1B. An OSL is the most difficult tendon or ligament to follow longitudinally to its insertion because the ligament extends diagonally from its origin to its insertion in two different planes. Following the medial or lateral OSL from its origin to the main body of OSL requires a transducer angle of about 45 degrees from the base of the PSBs to the palmar midline of the proximal phalanx. Properly aligning the transducer and eliminating off-normal incidence artifact is difficult. The OSLs may appear less echogenic because of an oblique orientation. The OSLs are thickest in the medial to lateral direction proximally. Each OSL measures 12 to 20 mm (lateral to

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medial) in the proximal aspect of P1A, decreasing to 9 to 17 mm just before their convergence, and 0 to 9 mm (one side only) at their insertion. The palmar to dorsal thickness of the OSLs is 5 to 12 mm in P1A, decreasing to 2 to 6 mm just proximal to the convergence, and decreasing again to 0 to 3 mm at the insertion. The mean CSA of an OSL determined with MRI is reported to be 0.86 cm2 in the proximal third, 0.56 cm2 in the middle third, and 0.40 cm2 in the distal third.19 However, there may be size differences between the medial and lateral OSLs.20

proximal phalanx to the insertion on the proximal palmar aspect of the middle phalanx. These ligaments are paired on the medial and lateral aspects of the pastern and are located by placing the transducer dorsal to the branch of the SDFT. The more abaxial branch originates first and is easier to follow than the more axial branch. Each branch has a round to oval shape, is homogeneously echogenic with a parallel fiber pattern, and must be followed individually from origin to insertion.

Straight Sesamoidean Ligament

The digital nerves are located dorsal to the lateral and medial aspects of the SDFT, adjacent to the lateral or medial palmar digital arteries.1 The nerves are found most easily by identifying the digital vein and artery, looking immediately adjacent (palmar) to the digital vein and the adjacent SDFT. The nerves are tiny, homogeneously echogenic circular structures. The normal thickness of the palmar or plantar digital nerves is 2 to 3 mm, with a CSA of 0.5 to 1 mm2.1

The origin of the SSL is found by angling the transducer in a proximal and dorsal direction from the proximal-most aspect of the pastern, just underneath the ergot, to image the ligament and the base of the PSBs. The SSL becomes a more oval-shaped structure and is palmar to the OSLs in zone P1B. The SSL remains dorsal to the DDFT as it inserts on the scutum medium. The dorsal-to-palmar thickness of the SSL gradually increases as the medial to lateral width decreases. The SSL measures 5 to 9 mm (palmar to dorsal) proximally, increasing slightly over the distal aspect of the proximal phalanx to 6 to 12 mm, and increasing again to 8 to 14 mm at the scutum medium. The medial-to-lateral thickness of the SSL ranges from 17 to 30 mm in zone P1A, decreases to 10 to 15 mm, and then widens over the scutum medium to 45 to 65 mm.3 The SSL is echogenic with normal parallel fiber alignment throughout, except at the insertion. A central symmetric hypoechoic area is commonly imaged in clinically normal horses at the insertion of the SSL.16 Care must be taken to be sure that lesions are not created at the insertion of the SSL because of the difficulty in aligning the transducer perpendicular to the ligamentous fibers owing to the horse’s heel. Comparison of this area with the contralateral normal limb should aid in determining whether a suspected lesion is real.

Cruciate Sesamoidean Ligaments

The cruciate sesamoidean ligaments are imaged only in the proximal-most portion of the pastern and measure 2 to 4 mm in a palmar to dorsal direction.3

Collateral Ligaments

The collateral ligaments of the proximal interphalangeal joint are easiest to examine by imaging in both longitudinal and transverse planes. The collateral ligaments of the proximal interphalangeal joint are homogeneously echogenic structures, with a parallel fiber pattern at the origin on the distal aspect of the proximal phalanx to the insertion on the proximal half of the middle phalanx.1,2

Proximal Interphalangeal Joint

The proximal interphalangeal joint is easiest to image initially in the longitudinal plane by identifying the joint space, and then a transverse evaluation of the joint can be made.7 Fluid normally is not imaged in the proximal interphalangeal joint.

Palmar/Plantar Ligaments of the Proximal Interphalangeal Joint

The palmar ligaments of the proximal interphalangeal joint can be imaged from the origin on the middle of the

Digital Nerves

TENDON AND LIGAMENT INJURIES In the fore pastern, the SDFT is the most frequently injured tendon or ligament in all performance horses.1-6,21 The OSLs are the second most commonly injured structures in the fore pastern, followed by injuries to the DDFT and SSL.1-6 In the hind pastern, injuries to the DDFT are most common, with a low incidence of injuries to the other tendonous and ligamentous structures.1-5 Injuries to the DDFT are accompanied most often by tenosynovitis of the DFTS.1-6 Injuries to the collateral ligaments of the proximal interphalangeal joint occur infrequently and are more common in the forelimb.1,3,7 Injuries to the palmar/plantar ligaments of the proximal interphalangeal joint are also uncommon and occur in forelimbs (most common) and hindlimbs. The tendonous and ligamentous structures in the pastern have little covering, and thus they are vulnerable to injury with puncture wounds and lacerations. Ultrasonographic evaluation of the pastern region in a horse with an acute laceration or puncture wound to the pastern should be performed aseptically and is an integral part of the evaluation of these soft tissue structures to determine whether injury occurred and the severity of the injury.

Superficial Digital Flexor Tendonitis

Injuries to the branches of the SDFT are more common in the forelimb.1-6,21,22 Injury in the pastern may occur in isolation, without an injury to the SDFT in the metacarpal or metatarsal region, or may be an extension of a more proximal tendon injury. Extension of the SDFT injury into the proximal pastern region, and less frequently into the mid and distal pastern, is more common in the forelimb. Abnormal conformation such as a long pastern, an underrun heel, or an axially displaced heel may predispose to injury of an SDFT branch. Lameness usually occurs at the onset of injury, is more common with SDFT injuries in the pastern than with those in the metacarpal or metatarsal region, and may persist longer, lasting for 1 to 4 weeks. Longitudinal swelling that extends in a proximal-to-distal direction along the lateral or medial aspect of the pastern throughout its length is often characteristic.1,2,21 Focal heat and sensitivity usually



Chapter 82  Soft Tissue Injuries of the Pastern

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A

Fig. 82-1  •  Ultrasonographic images of the right front medial branch of the superficial digital flexor tendon obtained in the proximal part of zone P1C in a horse with a recent injury. The anechoic to hypoechoic core lesion is apparent within the branch (arrows) in the transverse (left) and longitudinal (right) views. Fiber disruption and short linear fibers are imaged within the lesion in the longitudinal view, consistent with a recent injury and early healing. The horse was 1 of 5 degrees lame, with focal swelling, heat, and sensitivity to palpation.

accompany this swelling. However, in horses with acute injuries, no localizing clinical signs may be apparent, but lameness is alleviated by palmar (abaxial sesamoid) nerve blocks. Generally, swelling develops within 3 to 4 days. Ultrasonographic examination in the absence of swelling may result in false-negative results. Subluxation of the proximal interphalangeal joint can occur in horses with severe injury to or complete rupture of the SDFT in the pastern. Dropping of the fetlock joint with weight bearing can occur in horses with severe SDFT injury. Core injuries are the most common detected by ultrasonography (Figure 82-1), followed by diffuse injury to the affected branch.1,2 Complete ruptures or near complete ruptures of the branches do occur, but they are less frequent. These injuries can be unilateral or bilateral and uniaxial or biaxial, although uniaxial injuries are most common. The frequency of injury to the medial or lateral SDFT branch varies with the type of racing or sporting activity.21,22 Peritendonous soft tissue swelling is common. Avulsion fracture of the insertion of the SDFT branch occurs infrequently. Ultrasonographic evaluation of the more proximal aspect of the SDFT in the metacarpal or metatarsal region is indicated to determine whether the injury is an extension of a more proximal injury (see Chapter 69) (Figure 82-2). Ultrasonographic evaluation of the contralateral fore or hind pastern is recommended because bilateral disease may be present, more frequently in the forelimb. Radiological examination of the pastern is indicated for all horses with subluxation of the proximal interphalangeal joint, avulsion fractures at the insertion of the SDFT branch, or a ruptured SDFT branch. Treatment for horses with acute superficial digital flexor tendonitis in the pastern is similar to that in the metacarpal or metatarsal region.1,2 Horses with SDFT injuries in the pastern may have a poorer prognosis for returning to racing than those with injuries in the metacarpal region, with a more frequent recurrence of injury.1,2,22 Extension of the injury from the pastern to the metacarpal area may also occur, resulting in a shortened racing career.21 However,

B Fig. 82-2  •  Ultrasonographic images of the left superficial digital flexor tendon (SDFT) in the metacarpal region (A) and pastern (B) obtained from a horse with an acute severe injury to that tendon. This horse was lame at the walk, with substantial swelling of the SDFT in the metacarpal and pastern regions and heat and sensitivity of the tendon on palpation. The metacarpophalangeal joint dropped on weight bearing. A, The SDFT is enlarged (arrows) and contains a large central anechoic lesion completely lacking in tendon fibers. The SDFT was severely injured in the metacarpal region from 7 to 32 cm distal to the accessory carpal bone. The SDFT in zone 3C is surrounded by a thickened hypoechogenic digital flexor tendon sheath (DFTS). The transverse image is on the left, and the longitudinal image is on the right. B, The SDFT in zone P1A is markedly enlarged (arrows) with a central anechoic lesion that extended distally to the insertion of the lateral branch. The surrounding DFTS and peritendonous tissues are greatly thickened and hypoechogenic, and the distinction between the palmar margin of the SDFT and the peritendonous structures is difficult to discern. The lateral branch of the SDFT has nearly complete fiber disruption that extends to its insertion. The lateral side of the proximal pastern is the right image, and the medial side of the pastern is the left image. The SDFT and the DFTS were so enlarged that they could not be imaged in their entirety in a single image. Therefore the two halves of the SDFT were displayed together in these transverse images.

successful return to performance does occur for horses with SDFT branch injuries. Rare horses are able to continue to compete with SDFT branch injuries, without a period of rest, but these are the exceptions rather than the rule. Healing of the SDFT occurs similarly to that in the metacarpal region, with an increase in the echogenicity of the lesion and the subsequent appearance of short, usually randomly aligned linear echoes. Rehabilitation of horses with injuries to the SDFT branch is similar to that described for proximally located tendonitis and is based on the injury severity (see Chapter 69). A minimum of 6 months in a

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PART VIII  The Soft Tissues

Fig. 82-3  •  Ultrasonographic images of the left front lateral branch of the superficial digital flexor tendon obtained in zone P1B of a horse with a chronic healed core injury. The horse had sustained the original injury more than 5 years earlier, and after a long, controlled exercise program the horse had raced successfully several times a year, although some small areas of reinjury were detected periodically, necessitating short periods of downtime from race training. The original central core lesion is still visible in this branch as an echogenic central area, with a thin hypoechoic rim (arrow) in the transverse view (left) and longitudinal (right) views. In the longitudinal view, the central area of the tendon has a more random fiber pattern than the periphery (arrows).

controlled exercise program is needed for horses with mild SDFT branch injury, whereas 12 months or more are indicated for those with severe injury to the SDFT branch to maximize the horse’s chance of returning to its previous level of competition. Ultrasonographic monitoring of tendon healing is an important part of the rehabilitation program. A central echogenic scar surrounded by a hypoechoic halo may be detected in the SDFT branch with a healed core lesion (Figure 82-3). Peritendonous echogenic tissue representing immature and maturing fibrous tissue often is imaged adjacent to the injured SDFT branch and can result in adhesions between the branch and the surrounding tendonous and peritendonous structures. New areas of fiber disruption often occur adjacent to the previously healed area or are associated with adhesions to the surrounding tendonous or peritendonous structures.

Deep Digital Flexor Tendonitis

Deep digital flexor tendonitis is discussed in Chapter 70.

Distal Sesamoidean Desmitis Oblique Sesamoidean Desmitis

Desmitis of an OSL is the most common distal sesamoidean ligament injury and is seen in all types of performance horses.1-6 Horses with a valgus or varus limb conformation or a long sloping pastern may be at increased risk for OSL injuries. Swelling in the pastern region in horses with OSL injuries is characteristic because this ligament runs diagonally across the proximal to mid pastern, and swelling of the pastern usually occurs in this direction. Many horses have a boxy appearance to the fetlock joint from swelling at the origin of an OSL. Most horses have local swelling, heat, and pain detected on palpation of the affected ligament and lameness in the affected leg. However, some lesions restricted to the origin of the ligament occur without palpable abnormalities. Chronic injuries may be associated with dorsal enlargement of the dorsal articular margins of

Fig. 82-4  •  Ultrasonographic images of the origin of the left hind lateral oblique sesamoidean ligament (OSL) obtained in zone P1A. Most of the OSL is hypoechoic (arrow) in the transverse (left) and longitudinal (right) views (proximal is to the right). Substantial fiber disruption is visible in the longitudinal view, beginning at the base of the proximal sesamoid bone (arrow). There is no normal fiber pattern imaged at the origin of the lateral OSL. The more anechoic abaxial region represents a more recent injury, whereas the more echogenic area axially with a random fiber pattern represents a more chronic area of injury that is repairing. Some periligamentous echogenic soft tissue thickening surrounds the branch. The horse had a concurrent distal suspensory desmitis involving both suspensory branches that extended from 37 to 47 cm distal to the point of the hock. The horse was 2 of 5 degrees lame and had local heat, swelling, and mild sensitivity of the lateral OSL.

the proximal interphalangeal joint. Subluxation of the proximal interphalangeal joint can also occur in horses with either chronic injuries or complete rupture of the OSLs. This is characterized clinically by a dorsally convex profile of the pastern. Complete biaxial rupture of the OSLs is more common in Thoroughbreds and can have catastrophic implications. Injury to the medial OSL is more common than lateral OSL injury and is more common in the forelimb than in the hindlimb.3 Hindlimb OSL injuries are more common in nonracehorses. Horses with SL injury are also at increased risk of injuring the OSLs. Therefore ultrasonographic evaluation of the SL is recommended for all horses with oblique sesamoidean desmitis. Discrete core lesions often are seen in both OSLs, although diffuse areas of fiber damage and splits also occur (Figure 82-4). Injuries to the insertion of an OSL are usually diffuse (Figure 82-5). Periligamentous soft tissue thickening is often seen. Comparison of the ultrasonographic findings in the affected limb with the contralateral limb is recommended to be sure that subtle or early injuries are not missed. The origin and insertion of the OSLs should be carefully evaluated for avulsion fractures.1,2 Avulsion fractures usually occur in association with fiber tearing in the distal sesamoidean ligaments and occur from the base of the PSBs (Figure 82-6) and the insertion on the proximal phalanx. Avulsion fractures remain visible for years after the original injury, long after the associated desmitis in the distal sesamoidean ligament has resolved. Radiographs of the fetlock (particularly the PSBs) and the pastern regions should be obtained in all horses with OSL desmitis, paying careful attention to the base of the PSBs. However, it is important to recognize that entheseous new bone on the base of one or both of the PSBs or on the midpalmar aspect of the proximal phalanx can be seen as incidental radiological abnormalities, unassociated with lameness or active desmitis. Homogeneously radiodense mineralized bodies



Chapter 82  Soft Tissue Injuries of the Pastern

Fig. 82-5  •  Transverse (right) and longitudinal (left) ultrasonographic images of the right fore lateral oblique sesamoidean ligament (OSL) obtained where the two OSLs join. The lateral aspect of the transverse view is on the right side of the image. This horse had sustained an acute injury to the lateral OSL from the base of the lateral proximal sesamoid bone to its insertion. A large anechoic to hypoechoic core lesion (arrows) is visible. The horse was lame at the walk, with mild subluxation of the proximal interphalangeal joint and local swelling, heat, and sensitivity along the entire lateral OSL. DDFT, Deep digital flexor tendon; SSL, straight sesamoidean ligament; SDFT, superficial digital flexor tendon.

ligaments.25 Lesions characterized by an increase in size of an OSL and increased signal intensity in T1- and T2-weighted images can be seen as incidental findings in association with other primary causes of lameness.20 However, genuine primary lesions can be identified.19,23 Thirty-nine sports horses with pain localized to the fetlock region underwent MRI because conventional imaging techniques failed to yield a diagnosis.23 Injury of one or more of the distal sesamoidean ligaments was identified as the primary cause of lameness in 21 (54%) horses. Horses with acute injuries to the OSLs should be managed in the same way as those with other tendon and ligament injuries, with initial antiinflammatory therapy and exercise restriction.1,2 A controlled exercise program with incremental increases in the exercise level should be based on ultrasonographic monitoring. As the injury heals, the CSA of the ligament usually decreases, the echogenicity of the lesion increases, and linear echoes are imaged in the area of previous fiber tearing. A long recuperative period usually is indicated for horses with desmitis of an OSL to maximize the chance of return to athletic function. Prognosis for horses with OSL injury is guarded to grave for returning successfully to racing and other competitive athletic activities and depends on the severity of the injury. Horses with coexisting suspensory desmitis, basilar fractures of the PSBs, or subchondral palmar third metacarpal or plantar third metatarsal bone disease have a poorer prognosis for return to athletic function. The incidence of recurrence of OSL injury is high. Prognosis is grave for athletic horses with subluxation of the proximal interphalangeal joint associated with distal sesamoidean desmitis.

Straight Sesamoidean Desmitis

Fig. 82-6  •  Transverse (left) and longitudinal (right; proximal to the right) ultrasonographic images of the medial oblique sesamoidean ligament (OSL) obtained in zone P1A of the left forelimb in a horse with chronic active desmitis of the OSL and a small basilar sesamoid fracture. The hyperechogenic bony fragment (open arrow) is distracted away from the base of the proximal sesamoid bone (PSB) in the longitudinal view. Hyperechoic areas are visible  in the transverse view (large arrows), and areas of amorphous and random fiber pattern are imaged in the longitudinal view, proximal and distal to the fracture fragment. There is cortical irregularity of the base of the PSB (small arrows) in the longitudinal image. The horse was 1 of 5 degrees lame, with thickening of the base of the lateral PSB but no heat or local sensitivity.

are also sometimes seen distal to the PSBs as incidental findings. Since MRI has become used more frequently in the search for a diagnosis for horses with pain causing lameness localized to the fetlock or pastern region by diagnostic analgesia, the limitations of ultrasonography for injury diagnosis in the pastern have become more apparent.19,20,23 Injuries of the OSLs, SSL, and cruciate ligaments may be overlooked. Moreover, local analgesic techniques may be confusing. Pain associated with proximal lesions of these ligaments can be abolished by intraarticular analgesia of the fetlock or by intrathecal analgesia of the DFTS.23 However, care should be taken in the interpretation of signal intensity alterations on magnetic resonance images of the OSLs because of the magic angle effect,24 and the variable alignment of fibers in the proximal part of the

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Injuries to the SSL occur infrequently and may occur alone or with other soft tissue injuries.1-6 These injuries usually are associated with lameness, but focal heat, swelling, and sensitivity are not always detected. Lameness is usually acute in onset and may be severe. Some horses, especially those with proximal lesions, never develop localizing soft tissue swelling, and diagnosis depends on localizing pain to the pastern region by diagnostic analgesia and subsequent ultrasonographic identification of a lesion. The ease with which the most proximal aspect of the ligament can be seen depends on the conformation of the horse and the position of the ergot. Ultrasonographic evaluation of the SSL is most difficult in horses with short pasterns and easiest in those with relatively long, upright pasterns. Small splits or core lesions may be seen in the SSL.1-6 Large areas of fiber disruption in the SSL are uncommon (Figure 82-7). Areas of periosteal proliferative change or avulsion fractures at the insertion of the SSL on the proximal aspect of the middle phalanx may be seen (Figure 82-8). Avulsion fractures of the origin of the SSL are less common than with OSL desmitis, but the base of the PSBs should be evaluated carefully. Treatment for horses with SSL desmitis is similar to that recommended for horses with OSL desmitis.1-6 Horses with mild injuries have returned successfully to racing, but the prognosis for horses with more severe lesions is guarded for any form of competitive athletic function because recurrent injury is common. Horses with multiple tendonous or ligamentous injuries in the pastern have a guarded to grave prognosis for returning to full athletic function.

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PART VIII  The Soft Tissues ligament of the fetlock. Thickening of the proximal digital annular ligament and skin usually is substantial, with a combined thickness of 4 to 5 mm (normal thickness is 1 to 2 mm) and distention of the DFTS.21 Ultrasonographic evaluation of horses with proximal digital annular desmitis often reveals thickening of the synovium of the DFTS, in addition to the proximal digital annular ligament, and may reveal tendonitis of the SDFT or DDFT. Adhesions between the SDFT and the proximal digital annular ligament are suspected when restricted movement of the tendon relative to the proximal digital annular ligament is imaged during a dynamic examination.

Fig. 82-7  •  Ultrasonographic images of the right hind pastern obtained in zone P1A from a horse with an acute injury to the straight sesamoidean ligament (SSL). The horse was lame at the walk, with swelling of the proximal palmarolateral aspect of the pastern and local heat and sensitivity. The large anechogenic lesion (arrows) in the plantar aspect of the SSL is visible in the transverse view (left), with complete fiber disruption in this region that is best imaged on the longitudinal view (right). The SSL is mildly enlarged along the midline in the dorsal to palmar direction. Note also the markedly thickened subcutaneous tissues.

T

DDF

DDFT

Distal Digital Annular Desmitis

See Chapter 74 for a discussion of distal digital annular desmitis.

SOFT TISSUE SWELLING Soft tissue swelling in the pastern, without tendonous or ligamentous injury, can result from skin irritation caused by liniments, blisters, local therapeutic ultrasound or cold laser treatment, local trauma from a blow, bandaging, or bell (overreach) boots, or from a skin infection. Ultrasonographic findings of thickened anechogenic to echogenic subcutaneous tissues, with normal tendonous and ligamentous structures, are typical for injury or inflammation to the skin and subcutaneous tissues. Thickening of the skin also may be seen in horses with skin irritation or infection. These horses usually respond well to local or systemic antiinflammatory therapy.

TENOSYNOVITIS OF THE DIGITAL FLEXOR TENDON SHEATH Tenosynovitis of the DFTS is discussed in Chapter 74. Fig. 82-8  •  Ultrasonographic images of the left fore straight sesamoidean ligament (SSL) obtained in zone P1C-P2A from a horse with an acute  severe injury to the SSL and an avulsion of its insertion onto the scutum medium. The horse was lame at the walk, with subluxation of the proximal interphalangeal joint and substantial soft tissue swelling of the palmar pastern, with local heat and pain on palpation of the oblique sesamoidean ligament (OSL) and SSL. The hypoechoic lesion (small arrows) in the distalmost portion of the SSL and the hyperechogenic fragment distracted  away from the middle phalanx (large arrows) are visible in the transverse (right) and longitudinal (left) views. There is anechogenic effusion (open arrows) in the digital flexor tendon sheath. DDFT, Deep digital flexor tendon.

Cruciate Sesamoidean Desmitis

Desmitis of the cruciate sesamoidean ligaments is rare and difficult to diagnose by ultrasonography because of the location of these ligaments.1,2

Proximal Digital Annular Desmitis

Desmitis of the proximal digital annular ligament or proximal digital annular ligament constriction occurs infrequently (see Chapter 74).1,3 Affected horses usually have chronic moderate to severe lameness. Distention of the palmar pouch of the DFTS is usually present, in addition to subtle distention proximal to the palmar annular

ABNORMALITIES OF THE PASTERN JOINT Lameness and local swelling are two common findings in horses with injuries of the collateral or palmar ligaments of the proximal interphalangeal joint.1,3-5,7-9 Swelling is usually primarily medial and lateral, although it can be circumferential. Acute desmitis of the collateral ligaments may be confirmed by ultrasonography, with decreased echogenicity and loss of fiber pattern, with or without an associated avulsion fracture (Figure 82-9).1,3-5,7 In horses with more chronic injuries, enthesophyte formation at the origin and the insertion of the collateral ligaments usually is detected. A smoothing of these areas of insertional injury occurs as the desmitis becomes inactive. Similar ultrasonographic findings may be detected in horses with acute (Figure 82-10) and chronic injury (Figure 82-11) to the palmar ligaments of the pastern. These horses have a guarded prognosis for return to full athletic function. Bony proliferative changes associated with “high ringbone” are also easily imaged ultrasonographically.

NEURITIS/NEUROMA Neuritis of the palmar (plantar) digital nerves results in acute lameness associated with exquisite pain on palpation of the nerves and localized heat and swelling.



Chapter 82  Soft Tissue Injuries of the Pastern

Fig. 82-9  •  Longitudinal ultrasonographic images of the lateral collateral ligament of the proximal interphalangeal joint of the right hindlimb of horse with moderate lameness and localized swelling. The thickening of the lateral collateral ligament (large arrows), the hypoechoic areas of fiber disruption, and the short random fiber pattern seen in the longitudinal view are consistent with desmitis. The distal portion of the proximal phalanx is on the right side of both longitudinal images, and the proximal portion of the middle phalanx is on the left side of both images. The right image is the proximal portion of the lateral collateral ligament, and the left image is the distal portion of the ligament. The small anechoic slit between the proximal and middle phalanges represents the joint space (small arrow). There is marked bony proliferative change (irregular bone at the joint space), especially on the proximal aspect of the middle phalanx. Some echogenic subcutaneous thickening is present superficial to the collateral ligament.

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Fig. 82-11  •  Ultrasonographic images of the lateral palmar ligament of the proximal interphalangeal joint (large arrows) in a horse with chronic severe desmitis and severe enthesopathy. The bony proliferative changes of the proximal phalanx (small arrows) in the transverse (left) and longitudinal views (right) make imaging the ligament in its entirety in either plane impossible at the ligament’s origin. The visible portion of the ligament contains hypoechoic areas adjacent to the bony proliferative change in both views and near the ligament’s origin in the longitudinal view. The gelding was 2 of 5 degrees lame, with thickening over the lateral and medial aspects of the proximal phalanx, but no heat or local sensitivity was detected.

Fig. 82-10  •  Ultrasonographic images of the left abaxial plantar ligament of the proximal interphalangeal joint in a horse with severe desmitis associated with mild lameness and localized swelling. There is marked enlargement of the ligament. It is hypoechoic and circular to oval in the transverse view (left) and has a random fiber pattern in the longitudinal view (right). The arrows outline the margins of the ligament. A small amount of echogenic peritendonous subcutaneous tissue is visible.

Fig. 82-12  •  Transverse (left) and longitudinal (right) ultrasonographic images of the right fore medial palmar digital nerve obtained from a  horse with a neuroma resulting in acute onset of moderate lameness with local swelling, heat, and exquisite sensitivity to palpation. The enlarged nerve ending (arrows), oval to circular shape, is located palmar to the digital artery in the transverse view and superficial to the medial branch  of the superficial digital flexor tendon in both views. The cross-sectional area of the nerve is markedly increased. Anechoic and hypoechoic areas disrupt the nerve ending (arrows). Notice also the perineural soft tissue thickening.

Ultrasonography shows swelling and decreased echogenicity of the nerve (Figure 82-12). Neuromas following palmar digital neurectomy initially appear as focal painful swellings over the stump of the digital nerve. With ultrasonography, the nerve appears enlarged and hypoechoic,

with perineural soft tissue swelling in horses with an acute neuroma. The neuroma becomes more echogenic and heterogeneous with increasing chronicity of injury. A large amount of perineural echogenic tissue may be present in horses with chronic neuromas.

PART VIII  The Soft Tissues

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Skeletal Muscle   and Lameness Stephanie J. Valberg and Sue J. Dyson

normally present in high concentration within intact muscle cells but leak out into the bloodstream following cell damage. Three enzymes are used routinely to assess muscle necrosis: creatine kinase (CK), aspartate transaminase (AST), and lactate dehydrogenase (LDH). Serum myoglobin has also been used as a marker of acute muscle necrosis.2,3 The permeability of the muscle cell membrane, rate of enzyme production, alternate tissue sources of the enzyme, and rate of enzyme excretion/degradation may also influence serum enzyme activities.

Serum Creatine Kinase

DIAGNOSIS OF SPECIFIC MUSCLE DISORDERS IN THE HORSE Diagnosis of a particular muscle disorder is best accomplished with a thorough neuromuscular examination. The key components of the examination include the following.

History

A history of stiffness, muscle cramping, pain, muscle fasciculations, exercise intolerance, undiagnosed lameness, weakness, or muscle atrophy may all indicate a muscle disorder. Further characterization requires a detailed account of the horse’s performance level, exercise schedule, previous lameness, diet, vaccination history, signs of respiratory disease, duration, severity and frequency of muscle problem, any factors that initiate the muscle problem, and all medications with which the horse is being treated.

Physical Examination

References on page 1321

A detailed evaluation of the muscular system includes inspection of the horse for symmetry of muscle mass while standing with forelimbs and hindlimbs exactly square. Any evidence of fine tremors or fasciculations should be noted before palpating the horse. Horses originating in the southwestern United States that have muscle pain and fasciculations should have their ears examined with an otoscope for ear ticks (Otobius megnini).1 The entire muscle mass of the horse should be palpated for heat, pain, swelling, or atrophy comparing contralateral muscle groups. Firm, deep palpation of the lumbar, gluteal, and semi­membranosus and semitendinosus muscles may reveal pain, cramps, or fibrosis. The triceps, pectoral, gluteal, and semitendinosus muscles should be tapped with a fist or percussion hammer and observed for a prolonged contracture suggestive of myotonia. Running a blunt instrument such as artery forceps, a needle cap, or a pen over the lumbar and gluteal muscles should illicit extension (swayback), followed by flexion (hogback) in healthy horses. Guarding against movement may reflect abnormalities in the pelvic or thoracolumbar muscles, or pain associated with the thoracolumbar spine (see Chapter 52) or sacroiliac joints (see Chapter 51). The horse should be observed at the walk and the trot for any gait abnormalities, and some horses should be ridden.

Ancillary Diagnostic Tests Muscle Enzymes

Skeletal muscle necrosis may be identified by determining the activity in blood of serum enzymes or proteins that are

Isoforms of CK are found in skeletal muscle (MM), cardiac muscle (MB), and nervous tissue (BB). CK is a relatively low-molecular-weight protein (80,000 Da) that is intimately involved in energy production within the cell cytoplasm. It is liberated within hours of muscle damage, or increased cell membrane permeability, into the extracellular fluid and usually peaks at 4 to 6 hours after muscle injury (half-life [t 1 2] is 108 min).4 A threefold to fivefold increase in serum CK from normal values is believed to represent necrosis of approximately 20 g of muscle tissue.5 Rhabdomyolysis results in a proportionately greater increase in the MM isoform than the MB isoform, although some investigators disagree with the tissue specificity of serum CK isoforms in the horse.6 Limited elevations in CK (